Research integrity University Affairs

The Hupp and Ball Game

"Ted Hupp and Kathryn Ball may very well feel like kissing David Argyle on both cheeks."

Clare Francis said:

“Ted Hupp and Kathryn Ball may very well feel like kissing David Argyle on both cheeks.”

That’s because when the pseudonymous image integrity sleuth heard of David Argyle’s bullying and the cover-up by the University of Edinburgh in Scotland, UK, Clare Francis started to screen Argyle’s papers for image irregularities. And soon stumbled over Argyle’s postdoc Lisa Pang, who did her PhD at the Cancer Research UK (CRUK) Edinburg Centre and MRC Institute of Genetics & Molecular Medicine under Ted Hupp, the US-born Edinburgh professor, who proved to be Argyle’s collaborator.

Right away, Clare Francis found a treasure trove of questionable research papers from Hupp’s lab. From Hupp’s papers, the sleuth stumbled upon another Edinburgh professor, Kathryn Ball, and her lab’s papers proved a treasure trove as well!

Hupp and Ball are in fact a husband-and-wife team, they both started together as PhD students at the Michigan State University in USA, moved together as postdocs to Scotland, both to the University of Dundee lab of Sir David Lane (who is now at Karolinska Institutet in Stockholm, Sweden, and not replying to emails). Hupp and Ball then both became professors at the same Institute of Genetics and Cancer by CRUK and MRC in Edinburgh. Both work on cell cycle regulation, he on p53, she on the p21 protein. Both sit on the scientific advisory board of the Scottish biotech startup ILC Therapeutics which seeks to cure with interferon drugs various diseases including COVID-19. Both published, together and separately, Photoshopped stuff they should be deeply ashamed for, and both remained silent when I contacted them.

I want to celebrate this power couple.

Here is how Clare Francis was led to playing the Hupp and Ball game. From Argyle to Pang to Hupp to Ball.

Lisa Y. Pang, Mary Scott , Richard L. Hayward , Hisham Mohammed , C. Bruce A. Whitelaw, Graeme C.M. Smith , Ted R. Hupp p21(WAF1) is component of a positive feedback loop that maintains the p53 transcriptional program Cell Cycle (2011) doi: 10.4161/cc.10.6.15012

A Ponseau S blot image, “accidentally” reused, once in colour, once black-and-white, for two unrelated experiments. Why couldn’t the correct loading control be used? A mystery.

Here a paper by Hupp and Ball, rather old, raw data unavailable, but even Hupp agrees the gel is falsified:

Ashley Craig , Mary Scott , Lindsay Burch , Graeme Smith , Kathryn Ball, Ted Hupp Allosteric effects mediate CHK2 phosphorylation of the p53 transactivation domain EMBO reports (2003) doi: 10.1038/sj.embor.embor901

Hupp declared on PubPeer in June 2021:

The authors think that the apparent similarity resulted from image crop/paste from different gels to condense key data from Fig 1d of the same paper, but the original data are no longer available for analysis. This particular image does not affect the overall data interpretation or the conclusions from the study; regarding stimulation of the chk2 kinase using synthetic peptides (named 5 and 18) that are the best binders to chk2 (fig 1d) so that there is a correlation between binding of peptides to chk2 and chk2 stimulation; the same chk2 stimulatory peptides were also reproduced in other data throughout the paper in question and these same peptides were also used as kinase stimulators reproduced in a follow up study (10.1128/MCB.01595-06) and towards another regulatory protein (10.1016/j.molcel.2006.05.029 ).

Right-ho. It’s OK to fabricate results if you can reproduce them in your later papers. The first referenced study from Hupp’s lab has a blot duplication and a digitally assembled Chk1 gel, maybe the authors disapproved of the original results.

Ashley L. Craig , Jennifer A. Chrystal , Jennifer A. Fraser , Nathalie Sphyris , Yao Lin , Ben J. Harrison , Mary T. Scott , Irena Dornreiter , Ted R. Hupp The MDM2 ubiquitination signal in the DNA-binding domain of p53 forms a docking site for calcium calmodulin kinase superfamily members Molecular and Cellular Biology (2007) doi: 10.1128/mcb.01595-06

The second referenced paper by Hupp and Ball (Wallace et al 2006) hasn’t been yet commented upon on PubPeer, which under the circumstances of this story is no proof the paper is kosher.

What to make of the next paper though? Does any of this, uhm, reproducibility, affect the conclusions?

David Dornan , Mirjam Eckert , Maura Wallace, Harumi Shimizu, Eleanor Ramsay , Ted R. Hupp, Kathryn L. Ball Interferon regulatory factor 1 binding to p300 stimulates DNA-dependent acetylation of p53 Molecular and Cellular Biology (2004) doi: 10.1128/mcb.24.22.10083-10098.2004

The first author David Dornan is Hupp’s former PhD student and now Chief Scientific Officer of Bolt Therapeutics, where he “is working to harness the exciting technologies at Bolt to discover and develop therapeutics that may exploit myeloid cell biology to generate a robust anti-tumor immune response.” He also didn’t reply to my email, and neither did Bolt.

Here is another example of what Dornan learned in the Hupp lab:

David Dornan , Harumi Shimizu , Lindsay Burch , Amanda J. Smith , Ted R. Hupp The proline repeat domain of p53 binds directly to the transcriptional coactivator p300 and allosterically controls DNA-dependent acetylation of p53 Molecular and Cellular Biology (2003) doi: 10.1128/mcb.23.23.8846-8861.2003

Hupp replied to this finding in June 2021 on PubPeer that yes, the gel is digitally falsified, but it was just a control:

The authors feel that the apparent similarity likely resulted from mixing images cropped from different gels to assemble the final figure, but the original data could not be retrieved for analysis. This particular image was a negative control and does not affect the overall data interpretation or the conclusions from the study regarding interaction of p300 to proline-derived peptides, including deletion of the proline motifs of p53 that attenuate p300 functions (fig 5/6/7) and proline repeat domain protein promoter recruitment by chromatin ip (fig 8/9). The ability of proline repeat peptides to bind to p300 was also established by other studies (doi; 10.1074/jbc.M210696200; DOI; 10.1074/jbc.275.3.2115; DOI; 10.1016/j.jmb.2005.12.026; 10.1038/onc.2009.71).

Basically, controls are also there to prove that you didn’t fudge up your experiment to get the result you wanted. Hupp and his mentee Dornan failed the test.

In any case, more was found in the Dornan et al 2003 study:

There, Hupp didn’t reply anymore. Also, that Dornan et al 2003 paper shares western blots bands with another Dornan et al 2003 paper:

David Dornan , Harumi Shimizu , Neil D. Perkins , Ted R. Hupp DNA-dependent acetylation of p53 by the transcription coactivator p300 Journal of Biological Chemistry (2003) doi: 10.1074/jbc.m211460200 

Neil Perkins, now that name rings a bell. Alarm bells, actually. In 2014, Perkins, then with the Wellcome Centre of University of Dundee, retracted 4 papers, and explained in this regard to Retraction Watch that a) his postdoc Benjamin Barré did it and b) he, Perkins, exposed this fraud all by himself (OK, together with Barre’s PhD mentor). However, Perkins had already at that time several other papers flagged on PubPeer, and those were not co-authored by Barré.

Perkins’ academic career trajectory is interesting. Having spent 12 years as Dundee professor, he suddenly had enough and went to University of Bristol in 2008, but stopped being professor there after less than 2 years. Since 2010, Perkins is with University of Newcastle, where he is now deputy dean of biosciences. Meaning, all misconduct allegations in the faculty go through Perkins’ desk.

Between Hupp and Ball, the husband is the bigger academic heavyweight. In 2017, Hupp (together with a French colleague) received €9.5 Million from the Foundation for Polish Science to set up the International Centre for Cancer Vaccine Science at the University of Gdansk. Hupp runs the Centre’s Twitter account, here is his dear collaborator, the bully Argyle, visiting (right):

Any moment now will Dr Hupp’s Photoshop technology produce a cancer vaccine. Now let’s have a look at what Dr Ball’s lab enriched the science with.

Mary T Scott , Angela Ingram , Kathryn L Ball PDK1-dependent activation of atypical PKC leads to degradation of the p21 tumour modifier protein The EMBO Journal (2002) doi: 10.1093/emboj/cdf684

Maura Wallace used to head a unit at University of Edinburgh, a local newspaper once celebrated her receiving a charity donation for her cancer research. The charity money was put to good use.

Maura Wallace, Kathryn L. Ball Docking-dependent regulation of the Rb tumor suppressor protein by Cdk4 Molecular and Cellular Biology (2004) doi: 10.1128/mcb.24.12.5606-5619.2004

Well, at least we were spared Ball explaining on PubPeer that none of that data fabrication affected any conclusions, as her husband used to. Here a bit more of the Hupp and Ball game, courtesy of Clare Francis:

Jessica Pamment , Eleanor Ramsay , Michael Kelleher , David Dornan , Kathryn L Ball Regulation of the IRF-1 tumour modifier during the response to genotoxic stress involves an ATM-dependent signalling pathway Oncogene (2002) doi: 10.1038/sj.onc.1205981 
Ben Harrison , Michaela Kraus , Lindsay Burch , Craig Stevens , Ashley Craig , Phillip Gordon-Weeks , Ted R. Hupp DAPK-1 binding to a linear peptide motif in MAP1B stimulates autophagy and membrane blebbing Journal of Biological Chemistry (2008) doi: 10.1074/jbc.m706040200
Craig Stevens , Yao Lin , Ben Harrison , Lindsay Burch , Rachel A. Ridgway , Owen Sansom , Ted Hupp Peptide combinatorial libraries identify TSC2 as a death-associated protein kinase (DAPK) death domain-binding protein and reveal a stimulatory role for DAPK in mTORC1 signaling Journal of Biological Chemistry (2009) doi: 10.1074/jbc.m805165200 
M Wallace , P J Coates , E G Wright , K L Ball Differential post-translational modification of the tumour suppressor proteins Rb and p53 modulate the rates of radiation-induced apoptosis in vivo Oncogene (2001) doi: 10.1038/sj.onc.1204496 
Nicola J. MacLaine , Bodil Oster , Bettina Bundgaard , Jennifer A. Fraser , Carolyn Buckner , Pedro A. Lazo , David W. Meek , Per Höllsberg , Ted R. Hupp A central role for CK1 in catalyzing phosphorylation of the p53 transactivation domain at serine 20 after HHV-6B viral infection Journal of Biological Chemistry (2008) doi: 10.1074/jbc.m804433200

Now, you might say, well this all looks very serious. The University of Edinburgh sure won’t like it, a research misconduct investigation is probably already under way in full steam.

What are you, born yesterday and living the Moon? University of Edinburgh is not investigating anyone, in fact they refuse to admit any notifications of suspected research misconduct so they won’t have to open any investigations. Not on the dean of the veterinary faculty, the bully Argyle, and most certainly not on Hupp and Ball. Although, Edinburgh did investigate someone once, because the external pressure got too high and because the main perpetrator was a Bulgarian woman.

The senior lecturer Irina Stancheva was dismissed. All her partners in data forgery were absolved in full and enjoy their prestigious professorships at prestigious British universities on the virtue of being British males. Even Stancheva’s retractions were coordinated as not to hurt these important gentlemen.

The research integrity guidelines at Edinburgh state:

Professor Jonathan Seckl, Vice-Principal Planning, Resources and Research Policy, is the main responsible contact for Research Misconduct. Professor Seckl  delegates responsibility for research misconduct for each College.”

Seckl never replied to my notifications of course which bureaucratically means I never submitted anything. It is worth mentioning that Seckl is a collaborator of Moshe Szyf (here a questionable paper Weaver et al 2004), and also, the Edinburgh Vice-Principal can sympathise: his brother and Imperial College London professor Michael Seckl has a nice PubPeer record, including a retraction.

That retraction Michael Seckl earned together with Julian Downward, a somewhat controversial professor at The Crick. On the occasion of his other retraction, Downward explained to Retraction Watch that, let me check, yes, “Following a series of exhaustive London Research Institute (LRI) internal and external investigations, it was concluded” that also Dr Downward became a victim of a fraudulent foreigner he nourished at his bosom. A sad and tragic fate befalling many white British men of science.

There are no dirty foreigners to blame in our Hupp and Ball game (except yours truly), so you must understand why Michael Seckl’s brother Jonathan and his Edinburgh colleagues keep disregarding my email notifications. Plus, the Institute of Genetics and Molecular Medicine where Hupp and Ball work is part of College of Medicine and Veterinary Medicine, and its head Moira Whyte has vigorously defended Argyle from bullying complaints, including from a faculty member dying of cancer.

So you see, we up some hardened and ruthless opposition in Edinburgh. Don’t get fooled by the pictures of cuddly animals they deploy. These people will bite your head off if you get too close.

But evil as I am, I found a way in.

Edinburgh may refuse to admit my notification of suspected research misconduct, but I also contacted the University of Dundee, where the Hupp and Ball game originally began in the lab of Sir David Lane. I did this recalling how in 2016 Dundee cracked down on the science fraud by their former lecturer Robert Ryan. Ryan was made to resign, his funding withdrawn, and that despite Ryan’s alma mater University College Cork in Ireland aggressively defending his research, determined to protect at all costs their professor and Ryan’s mentor (and co-author) Maxwell Dow.

So I sent the PubPeer evidence to the University of Dundee, Right away, my notification was acknowledged with this message from Paul Davies, one of university’s research integrity leads:

Thank you very much for raising this with the School of Life Sciences Research Integrity Group. As an Institution, we are proactively engaged in Research Integrity matters: we deal with the underlying causes of reproducibility issues in research and thoroughly evaluate all concerns and allegations of research misconduct involving our current and former researchers. We subscribe to PubPeer alerts (in fact we worked with PubPeer to enable searching by institution) and react to each one involving the University of Dundee.  We are aware of the published comments you highlight and we are currently looking at these and will evaluate them thoroughly.

Davies then announced to inform “all stakeholders, including the Journals, to establish the facts.” Which will first and foremost include the University of Edinburgh. Maybe Jonathan Seckl will have to grudgingly allow an investigation after all. Expect no misconduct findings though!

Photos: T. Hupp/Twitter, University of Edinburgh

Nobody in Edinburgh is answering emails, and neither does Hupp’s and Ball’s mentor Sir David Lane in Stockholm. He should though, even one of his own papers is affected.

Kathryn L. Ball, David P. Lane Human and plant proliferating-cell nuclear antigen have a highly conserved binding site for the p53-inducible gene product p21WAF1 European Journal of Biochemistry (1996) doi: 10.1111/j.1432-1033.1996.0854p.x


114 comments on “The Hupp and Ball Game

  1. “[Jonathan] Seckl never replied to my notifications of course which bureaucratically means I never submitted anything. It is worth mentioning that Seckl is a collaborator of Moshe Szyf (here a questionable paper Weaver et al 2004)..”

    This paper:

    https://pubpeer.com/publications/B8213982BA13202EF2157FC41755BC

    Cited 6574 times as of 02.01.2022 according to Google Scholar.

    https://scholar.google.co.uk/scholar?hl=en&as_sdt=0%2C5&q=seckl+meaney+2004&oq=seckl+meaney

    Like

  2. Chief Publishing Officer “Frontiers”, Mirjam Eckert, is author of a problematic publication with Ted Hupp and Kathryn Ball.

    This paper:- https://pubpeer.com/publications/16180CE2482CFEBD624AEF605B1D20

    Problematic data figures:-

    2A, much more similar after vertical compression than expected.

    3A, much more similar than expected,

    3B, much more similar after horizontal flip than expected,

    6B in itself and,

    also, data in figure 6B seems to come from an earlier paper.

    https://ch.linkedin.com/in/mirjam-eckert-ab391519/en

    Experience
    Frontiers
    Frontiers
    8 years 1 month

    Chief Publishing Officer
    Nov 2020 – Present1 year 3 months

    Lausanne, Vaud, Switzerland

    Publishing Director
    Jan 2019 – Nov 20201 year 11 months

    Lausanne Area, Switzerland

    Editorial Director
    Mar 2016 – Dec 20182 years 10 months

    Lausanne und Umgebung, Schweiz

    Editorial Office Manager
    Nov 2014 – Mar 20161 year 5 months

    Lausanne und Umgebung, Schweiz

    Journal Manager
    Jan 2014 – Oct 201410 months

    Lausanne

    Education
    The University of Dundee

    The University of Dundee Graphic
    The University of Dundee
    Doctor of Philosophy (PhD)Molecular Oncology
    2002 – 2006

    Like

  3. https://timesofmalta.com/articles/view/new-scientific-partnership-to-create-opportunities-for-cancer-research.866181

    21 April 2021 Times of Malta

    “Research Minister Owen Bonnici and Education Minister Justyne Caruana gave details about this collaboration, which aims at sharing new knowledge that results in innovative ways to treat cancer for immunotherapy to become more precise, personalised, and effective.”

    “This scientific partnership was established thanks to the long-standing collaboration between David Saliba from the University of Malta and Ted Hupp, the director of the ICCVS.”

    Research Minister Owen Bonnici and Education Minister Justyne Caruana should ask to see Ted Hupp’s data.

    Like

  4. Oncogene . 1998 Oct 1;17(13):1691-703. doi: 10.1038/sj.onc.1202104.

    Cell cycle arrest and DNA endoreduplication following p21Waf1/Cip1 expression

    S Bates 1, K M Ryan, A C Phillips, K H Vousden

    Affiliation
    1
    ABL Basic Research Program, NCI-FCRDC, Frederick, Maryland 21702-1201, USA.
    PMID: 9796698 DOI: 10.1038/sj.onc.1202104

    Problematic data figure 3(b). Much more similar than expected.

    Pubpeer comments: https://pubpeer.com/publications/A0F7A3FFD9F1D6D44D149007691B32

    K H Vousden presently: https://www.crick.ac.uk/research/find-a-researcher/karen-vousden

    “moving back to the NCI in 1995, where she was Director of the Molecular Virology and Carcinogenesis Section at the ABL-Basic Research programme and then Chief of the Regulation of Cell Growth Laboratory.

    In 2002, she returned to the UK to become the Director of the CRUK Beatson Institute in Glasgow, moving back to London in 2016 to take up the role of Chief Scientist at CRUK and Group Leader at the Francis Crick Institute.”

    K M Ryan presently: https://www.beatson.gla.ac.uk/Cancer-Metabolism-Growth-and-Survival/kevin-ryan-tumour-cell-death.html

    Like

  5. Reply to Leonid Schneider
    January 8, 2022

    I think it is like that. Occupy the leading positions, fuck the science!

    Like

  6. Cell Signal. 2015 Sep;27(9):1816-23. doi: 10.1016/j.cellsig.2015.05.017. Epub 2015 Jun 9.

    p70S6K is regulated by focal adhesion kinase and is required for Src-selective autophagy

    Emma Sandilands 1, Christina Schoenherr 1, Margaret C Frame 2

    Affiliations

    1Edinburgh Cancer Research UK Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road South, Edinburgh EH4 2XR, United Kingdom.

    2Edinburgh Cancer Research UK Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road South, Edinburgh EH4 2XR, United Kingdom.

    Electronic address: m.frame@ed.ac.uk.

    PMID: 26071201 PMCID: PMC4508348 DOI: 10.1016/j.cellsig.2015.05.017

    Figure 1C. Much more similar than expected.

    https://pubpeer.com/publications/128DB19432DF58596B3402D4F33AB6

    Like

  7. https://www.ed.ac.uk/cancer-centre/research/myant-group

    2008
    LSH Cooperates with DNA Methyltransferases To Repress Transcription
    Myant, K. & Stancheva, I., Jan 2008, In: Molecular and Cellular Biology. 28, 1, p. 215-226 12 p.
    Research output: Contribution to journal › Article › peer-review

    https://pubpeer.com/publications/63AED75DBD88BDDCF45E2AB23949F5

    Figure 6B. Much more similar than expected.

    Like

  8. “The senior lecturer Irina Stancheva was dismissed. All her partners in data forgery were absolved in full and enjoy their prestigious professorships at prestigious British universities on the virtue of being British males.”

    https://www.artcraftcollective.co.uk/artists/irina-stancheva-studio-523-fused-glass-artist/

    Irina Stancheva Studio 523 Fused Glass Artist

    “After working in academic science for more than 20 years, I decided to try something new and exciting. I set up a studio for fused glass work and now I am having a lot of fun designing and making variety of fused glass objects and jewellery.

    Glass is an amazing material, which interacts with light in many interesting ways and offers infinite possibilities to explore combinations of colors, transparency, shape and texture. My science background also comes useful when considering chemical reactions that occur between different kinds of glass and metals when they melt and blend with each other in the kiln. My fused glass creations are inspired by nature and often by what I see when I walk to my studio.

    I am happy to teach anyone in my studio, so get in touch if you are interested in fused glass and would like to make something beautiful.”

    We have a range of Irina’s work in the Gallery, from hanging ‘fish’ to tealight holders, decorative (and practical) plates and bowls.

    Irina is also more than happy to discuss commissions so please contact her directly or through the Gallery.”

    Might Kathryn Ball and Ted Hupp consider fused glass?

    Note that Irina Stancheva writes:

    “I am happy to teach anyone in my studio, so get in touch if you are interested in fused glass and would like to make something beautiful”.

    Like

  9. Mol Cancer Ther . 2003 Nov;2(11):1121-8.

    Replication and episomal maintenance of Epstein-Barr virus-based vectors in mouse embryonal fibroblasts enable synthetic lethality screens

    https://mct.aacrjournals.org/content/2/11/1121.article-info

    AUTHOR INFORMATION

    Yulia Einav 1, Elena Shistik 1, Michal Shenfeld 1, Arnold H. Simons 1, David W. Melton 2 and Dan Canaani 1

    1Department of Biochemistry, The George S. Wise Faculty of Life Sciences, Tel Aviv University, Ramat Aviv, Israel and

    2Sir Alastair Currie Cancer Research UK Laboratories, Molecular Medicine Centre, University of Edinburgh, Edinburgh, UK

    Requests for Reprints: Dan Canaani, Department of Biochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Ramat Aviv 69978, Israel. Phone: 972-3-6408985; Fax: 972-3-6424270. E-mail: canaani@post.tau.ac.il

    PMID: 14617785

    Problematic data figures 2A and 2B.

    Figure 2A. Much more similar than expected.

    Figure 2B. Much more similar than expected.

    Like

  10. Mol Cell Biol . 2003 Dec;23(24):9245-50. doi: 10.1128/MCB.23.24.9245-9250.2003.

    While K-ras is essential for mouse development, expression of the K-ras 4A splice variant is dispensable

    Sarah J Plowman 1, D James Williamson, Maureen J O’Sullivan, Jennifer Doig, Ann-Marie Ritchie, David J Harrison, David W Melton, Mark J Arends, Martin L Hooper, Charles E Patek

    Affiliation
    1
    Sir Alastair Currie Cancer Research UK Laboratories, Molecular Medicine Centre, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, Scotland, U.K.

    PMID: 14645534 PMCID: PMC309700 DOI: 10.1128/MCB.23.24.9245-9250.2003

    Problematic data figure 4, middle panel, much more similar than expected.

    Like

    • Additional problematic data Mol Cell Biol . 2003 Dec;23(24):9245-50. doi: 10.1128/MCB.23.24.9245-9250.2003.

      Problematic data figure 2B. Much more similar than expected.

      Like

    • More problematic data figure 4 Mol Cell Biol . 2003 Dec;23(24):9245-50. doi: 10.1128/MCB.23.24.9245-9250.2003.

      Figure 4, middle panel. Much more similar than expected. This time inside the light blue rectangles.

      Like

    • Yet more problematic data figure 4 Mol Cell Biol . 2003 Dec;23(24):9245-50. doi: 10.1128/MCB.23.24.9245-9250.2003.

      Problematic data figure 4 bottom panel. Much more similar than expected.

      Like

    • Exp Cell Res . 2006 Jan 1;312(1):16-26. doi: 10.1016/j.yexcr.2005.10.004. Epub 2005 Nov 4.

      The K-Ras 4A isoform promotes apoptosis but does not affect either lifespan or spontaneous tumor incidence in aging mice

      Sarah J Plowman 1, Mark J Arends, David G Brownstein, Feijun Luo, Paul S Devenney, Lorraine Rose, Ann-Marie Ritchie, Rachel L Berry, David J Harrison, Martin L Hooper, Charles E Patek

      Affiliation
      1
      Sir Alastair Currie Cancer Research UK Laboratories, Molecular Medicine Centre, The University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK.
      PMID: 16271715 DOI: 10.1016/j.yexcr.2005.10.004

      Problematic data figure 1B. Much more similar than expected.

      Like

  11. Data in Nucleic Acids Res. 2001 Nov 15; 29(22): 4541–4550 reappears in

    Transgenic Res . 2011 Feb;20(1):109-22. doi: 10.1007/s11248-010-9396-3. Epub 2010 Apr 21.

    The  figure 1 legend Transgenic Res . 2011 Feb;20(1):109-22 does not state that the data have appeared earlier. 

    Transgenic Res . 2011 Feb;20(1):109-22 claims to be an ORIGINAL PARER.

    The text of Transgenic Res . 2011 Feb;20(1):109-22 does mention Selfridge et al. 2001 in the text, but does not state that the data are the same.

    “A panel of tissues from a wild-type BALB/c adult male mouse was analysed by Northern blotting using an Ercc1 cDNA probe (Probe a in Selfridge et al. 2001).”

    1. Nucleic Acids Res. 2001 Nov 15; 29(22): 4541– 4550.doi: 10.1093/nar/29.22.4541PMCID: 
    PMC92547PMID: 11713303

    Correction of liver dysfunction in DNA repair-deficient mice with an ERCC1 transgene

    Jim Selfridge, Kan-Tai Hsia, Nicola J. Redhead,1 and David W. Melton1,a

    Author information 

    Institute of Cell and Molecular Biology, University of Edinburgh, King’s Buildings, Mayfield Road, Edinburgh EH9 3JR, UK and 

    1Sir Alastair Currie CRC Laboratories, Molecular Medicine Centre, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK

    a To whom correspondence should be addressed. Tel: +44 131 651 1079; Fax: +44 131 651 1072;

    Email: david.melton@ed.ac.uk

    Present address: Kan-Tai Hsia, Faculty of Dentistry, National Yang-Ming University, Taiwan, Republic of China.

     2. Transgenic Res . 2011 Feb;20(1):109-22. doi: 10.1007/s11248-010-9396-3. Epub 2010 Apr 21.

    A novel transcript for DNA repair gene Ercc1 in mouse skin

    L Song 1, A G Winter, J Selfridge, D W Melton

    Affiliations 

    1Institute of Genetics and Molecular Medicine, MRC Human Genetics Unit, Western General Hospital, University of Edinburgh, Crewe Road, Edinburgh, EH4 2XU, UK.

    PMID: 20407824 DOI: 10.1007/s11248-010-9396-3

    Like

  12. J Mol Biol . 2004 Mar 12;337(1):115-28. doi: 10.1016/j.jmb.2003.10.081.

    Phage-peptide display identifies the interferon-responsive, death-activated protein kinase family as a novel modifier of MDM2 and p21WAF1

    Lindsay R Burch 1, Mary Scott, Elizabeth Pohler, David Meek, Ted Hupp

    Affiliation
    1
    Cancer Research UK Laboratories, Department of Molecular and Cellular Pathology, University of Dundee, Dundee DD1 9SY, Scotland, UK.
    PMID: 15001356 DOI: 10.1016/j.jmb.2003.10.081

    Problematic data figure 4D. Vertical, straight change in signal between – and + lanes. There are only 2 lanes.

    Like

  13. Mol Cell Biol. 2002 Jul; 22(14): 5141–5156.doi: 10.1128/MCB.22.14.5141-5156.2002PMCID: PMC139773PMID: 12077342

    Mammalian PRP4 Kinase Copurifies and Interacts with Components of Both the U5 snRNP and the N-CoR Deacetylase Complexes

    Graham Dellaire,1 Evgeny M. Makarov,2 JeffJ.M. Cowger,3 Dasa Longman,1 Heidi G. E. Sutherland,1 Reinhard Lührmann,2 Joseph Torchia,3 and Wendy A. Bickmore1,*

    Author information 
    MRC-Human Genetics Unit, Western General Hospital, Edinburgh, United Kingdom,1

    Department of Cellular Biochemistry, Max-Planck-Institute for Biophysical Chemistry, Gottingen, Germany,2 

    and Toxicology and Oncology, Cancer Research Laboratories, London Regional Cancer Centre, The University of Western Ontario, London, Ontario, Canada3

    *Corresponding author. Mailing address: MRC-Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom. Phone: 44 (131) 467-8418. Fax: 44 (131) 343-2620.
    E-mail: Wendy.Bickmore@hgu.mrc.ac.uk

    Presently:https://www.ed.ac.uk/profile/wendy-bickmore

    Professor Wendy Bickmore (FRS FMedSci FRSE)
    Director – MRC Human Genetics Unit
    Email: hgu.director@ed.ac.uk

    Problematic data figure 5C. Much more similar than expected. Also, vertical, straight change in signal in one panel, but not in the other.

    Problematic data figure 8B. Much more similar than expected.

    Problematic data figure 5A. Vertical, straight change in signal in one panel, but not in the other.

    Like

    • Science. 1992 Jul 10;257(5067):235-7. doi: 10.1126/science.1321494.

      Modulation of DNA binding specificity by alternative splicing of the Wilms tumor wt1 gene transcript

      W A Bickmore 1, K Oghene, M H Little, A Seawright, V van Heyningen, N D Hastie

      Affiliation
      1Medical Research Council Human Genetics Unit, Western General Hospital, Edinburgh, Scotland.
      PMID: 1321494 DOI: 10.1126/science.1321494

      Figure 4. Vertical, straight line between lanes 2 and 3 in +P2 panel, and vertical, straight line/change in background between lanes 3 and 4 in +P5 panel. This makes it less clear of the Electrophoretic mobility-shift assays in those panels have been run in the same gel. It was more common to splice data in those days, but for reasons such as running out of lanes. There are only 4 lanes in each of the panels shown.

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  14. Mol Biol Cell 2009 Mar;20(6):1845-54. doi: 10.1091/mbc.e08-09-0944. Epub 2009 Jan 21.

    The hydrophobic cysteine-rich domain of SNAP25 couples with downstream residues to mediate membrane interactions and recognition by DHHC palmitoyl transferases

    Jennifer Greaves 1, Gerald R Prescott, Yuko Fukata, Masaki Fukata, Christine Salaun, Luke H Chamberlain

    Affiliation
    1Centre for Integrative Physiology, School of Biomedical Sciences, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom.

    PMID: 19158383 PMCID: PMC2655257 DOI: 10.1091/mbc.e08-09-0944

    Figure 9. Much more similar than expected.

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  15. Nat Genet . 2010 Jan;42(1):89-93. doi: 10.1038/ng.494. Epub 2009 Dec 20.

    Wt1 is required for cardiovascular progenitor cell formation through transcriptional control of Snail and E-cadherin

    Ofelia M Martínez-Estrada 1, Laura A Lettice, Abdelkader Essafi, Juan Antonio Guadix, Joan Slight, Víctor Velecela, Emma Hall, Judith Reichmann, Paul S Devenney, Peter Hohenstein, Naoki Hosen, Robert E Hill, Ramón Muñoz-Chapuli, Nicholas D Hastie

    Affiliation
    1
    MRC Human Genetics Unit and Institute for Genetics and Molecular Medicine, Edinburgh, UK.
    PMID: 20023660 PMCID: PMC2799392 DOI: 10.1038/ng.494

    Problematic data figure 2i. Much more similar than expected.

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    • Cardiovasc Res . 2005 Feb 1;65(2):328-33. doi: 10.1016/j.cardiores.2004.11.015.

      Human adipose tissue as a source of Flk-1+ cells: new method of differentiation and expansion

      Ofelia María Martínez-Estrada 1, Yolanda Muñoz-Santos, Josep Julve, Manuel Reina, Senén Vilaró

      Affiliations

      1Departament de Biologia Cellular, Facultat Biologia, Universitat de Barcelona, Ave Diagonal, 645 E-08028 Barcelona, Spain.

      ofeliamartinez@ub.eduPMID

      15639471 DOI: 10.1016/j.cardiores.2004.11.015

      Figures 2C and 2D size of cell clusters does not appear to be bigger (just a higher magnification).

      Like

    • Biochem J . 2006 Mar 1;394(Pt 2):449-57. doi: 10.1042/BJ20050591.

      The transcription factors Slug and Snail act as repressors of Claudin-1 expression in epithelial cells

      Ofelia M Martínez-Estrada 1, Albert Cullerés, Francesc X Soriano, Hector Peinado, Victoria Bolós, Fernando O Martínez, Manuel Reina, Amparo Cano, Myriam Fabre, Senén Vilaró

      Affiliation
      1Departament de Biologia Cellular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain.

      ofeliamartinez@ub.edu

      PMID: 16232121

      https://pubpeer.com/publications/0BE518183A2869E59EE898BA4426CE

      Figure 5. Much more similar than expected.

      Figure 2F. Much more similar than expected.

      Like

  16. Spot the difference!

    Ann N Y Acad Sci . 2004 Dec;1032:63-84. doi: 10.1196/annals.1314.006.
    Glucocorticoid programming
    Jonathan R Seckl 1, Michael J Meaney

    Affiliation
    1Endocrinology Unit, University of Edinburgh, Molecular Medicine Centre, Western General Hospital, Edinburgh, EH4 2XU, UK. J.Seckl@ed.ac.uk
    PMID: 15677396
    DOI: 10.1196/annals.1314.006

    Abstract
    Epidemiological evidence suggests that an adverse fetal environment permanently programs physiology, leading to increased risks of cardiovascular, metabolic, and neuroendocrine disorders in adulthood. Prenatal glucocorticoid excess or stress might link fetal maturation and adult pathophysiology. In a variety of animal models, prenatal glucocorticoid exposure or inhibition of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the fetoplacental “barrier” to maternal glucocorticoids, reduces birth weight and causes permanent hypertension, hyperglycemia, and increased hypothalamic-pituitary-adrenal axis (HPA) activity and behavior resembling anxiety. In humans, 11beta-HSD2 gene mutations cause low birth weight and reduced placental 11beta-HSD2 activity associated with intrauterine growth retardation. Low birth weight babies have higher plasma cortisol levels throughout adult life, indicating HPA programming. The molecular mechanisms may reflect permanent changes in the expression of specific transcription factors; key is the glucocorticoid receptor itself. Differential programming of the glucocorticoid receptor in different tissues reflects effects upon one or more of the multiple tissue-specific alternate first exons/promoters of the glucocorticoid receptor gene. Overall, the data suggest that either pharmacological or physiological exposure to excess glucocorticoids prenatally programs pathologies in adult life.

    Eur J Endocrinol . 2004 Nov;151 Suppl 3:U49-62. doi: 10.1530/eje.0.151u049.
    Prenatal glucocorticoids and long-term programming
    Jonathan R Seckl 1

    Affiliation
    1Endocrinology Unit, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, UK. J.Seckl@ed.ac.uk
    PMID: 15554887
    DOI: 10.1530/eje.0.151u049

    Abstract
    Epidemiological evidence suggests that low birth weight is associated with an increased risk of cardiovascular, metabolic and neuroendocrine disorders in adult life. Glucocorticoid administration during pregnancy reduces offspring birth weight and alters the maturation of the lung and other organs. We hypothesised that prenatal exposure to excess glucocorticoids or stress might represent a mechanism linking foetal growth with adult pathophysiology. In rats, birth weight is reduced following prenatal exposure to the synthetic steroid dexamethasone, which readily crosses the placenta, or to carbenoxolone, which inhibits 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the physiological feto-placental ‘barrier’ to maternal glucocorticoids. As adults, the offspring exhibit permanent hypertension, hyperglycaemic, increased hypothalamic-pituitary-adrenal (HPA) axis activity and behaviour reminiscent of anxiety. Physiological variations in placental 11beta-HSD2 activity correlate directly with foetal weight. In humans, 11beta-HSD2 gene mutations cause low birth weight. Moreover, low-birth-weight babies have higher plasma cortisol levels throughout adult life, indicating HPA axis programming. The molecular mechanisms may reflect permanent changes in the expression of specific transcription factors, key among which is the glucocorticoid receptor (GR) itself. The differential programming of the GR in different tissues reflects effects upon one or more of the multiple tissue-specific alternate first exons/promoters of the GR gene. Overall, the data suggest that both pharmacological and physiological exposure prenatally to excess glucocorticoids programmes cardiovascular, metabolic and neuroendocrine disorders in adult life.

    Like

  17. “Professor Jonathan Seckl, Vice-Principal Planning, Resources and Research Policy, is the main responsible contact for Research Misconduct. Professor Seckl delegates responsibility for research misconduct for each College.”

    Spot the difference!

    Ann N Y Acad Sci . 2004 Jun;1024:182-212. doi: 10.1196/annals.1321.099.
    Early environmental regulation of hippocampal glucocorticoid receptor gene expression: characterization of intracellular mediators and potential genomic target sites
    Ian C G Weaver 1, Josie Diorio, Jonathan R Seckl, Moshe Szyf, Michael J Meaney

    Affiliation
    1McGill Program for the Study of Behavior, Genes and Environment, Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Montreal, Quebec, Canada.
    PMID: 15265782 DOI: 10.1196/annals.1321.099

    Abstract
    Environmental conditions in early life permanently alter the development of glucocorticoid receptor gene expression in the hippocampus and hypothalamic-pituitary-adrenal responses to acute or chronic stress. In part, these effects can involve an activation of ascending serotonergic pathways and subsequent changes in the expression of transcription factors that might drive glucocorticoid receptor expression in the hippocampus. This paper summarizes the evidence in favor of these pathways as well as recent studies describing regulatory targets within the chromatin structure of the promoter region of the rat hippocampal glucocorticoid receptor gene.

    Mol Cell Endocrinol. 2001 Dec 20;185(1-2):205-18. doi: 10.1016/s0303-7207(01)00635-9.
    Early environmental regulation of hippocampal glucocorticoid receptor gene expression: characterization of intracellular mediators and potential genomic target sites
    I C Weaver 1, P La Plante, S Weaver, A Parent, S Sharma, J Diorio, K E Chapman, J R Seckl, M Szyf, M J Meaney

    Affiliation
    1McGill program for the Study of Behavior, Genes and Environment, Douglas Hospital Research Centre, Department of Psychiatry, McGill University, 6875 LaSalle Blvd., Montreal, Quebec, Canada H4H 1R3.
    PMID: 11738810 DOI: 10.1016/s0303-7207(01)00635-9

    Abstract
    Environmental conditions in early life permanently alter the development of glucocorticoid receptor gene expression in the hippocampus and hypothalamic-pituitary-adrenal responses to acute or chronic stress. In part, these effects can involve an activation of ascending serotonergic pathways and subsequent changes in the expression of transcription factors that might drive glucocorticoid receptor expression in the hippocampus. This paper summarizes the evidence in favor of these pathways as well as recent studies describing regulatory targets on the promoter region of the rat hippocampal glucocorticoid receptor gene.

    Like

    • “Professor Jonathan Seckl, Vice-Principal Planning, Resources and Research Policy, is the main responsible contact for Research Misconduct. Professor Seckl delegates responsibility for research misconduct for each College.”

      PLoS One . 2013 Sep 26;8(9):e75874. doi: 10.1371/journal.pone.0075874. eCollection 2013.

      Pro-inflammatory cytokine induction of 11β-hydroxysteroid dehydrogenase type 1 in A549 cells requires phosphorylation of C/EBPβ at Thr235

      Cristina L Esteves 1, Manu Verma, Ewa Róg-Zielińska, Val Kelly, Shuji Sai, Amandine Breton, Francesc X Donadeu, Jonathan R Seckl, Karen E Chapman

      Affiliation
      1
      Endocrinology Unit, University/BHF Centre for Cardiovascular Science, Queen’s Medical Research Institute, The University of Edinburgh, Edinburgh, United Kingdom.
      PMID: 24086653 PMCID: PMC3784397 DOI: 10.1371/journal.pone.0075874

      Problematic data figure 3A. Much more similar than expected.

      Like

  18. “A Ponseau S blot image, “accidentally” reused, once in colour, once black-and-white, for two unrelated experiments. Why couldn’t the correct loading control be used? A mystery.”

    https://pubpeer.com/publications/8CE988307EBAA1F791A99AB678C107

    https://pubpeer.com/publications/8CE988307EBAA1F791A99AB678C107#2

    The authors agree this data is duplicated. These are both coomassie blue gels (Figure 8M and Figure 10N), used not as a loading controls per se, but to give an overall barcode of the total protein constellation in each of the subcellular fractions F1-F4. The differences in the barcodes in each of the lanes shows that the chemical fractionation was working. This duplication does not alter the outcome of the immunoblot interpretation in the figures 8 and 10, which shows differences in p53 and p21 re-distribution into different subcellular compartments, as a function of targeted p21 siRNA treatment (Figure 8K and 8L) or as a function of ATM inhibition Figure 10 (L and M). Nevertheless, because the original raw coomassie blue gels have been traced (attached images), we now know that Figure 8M is in the appropriate position but that Figure 10N contains the wrong commassie blue control. The original paper should have inserted the Figure 10 (attached) and communication with the Journal will be initiated to issue an author correction.

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  19. Re: https://www.gla.ac.uk/researchinstitutes/cancersciences/staff/maryscott/

    Research Associate (Paul O’Gorman Leukaemia Research Centre)telephone: 01413302606

    email: Mary.Scott@glasgow.ac.uk

    Wolfson Wohl Cancer Research Centre, Garscube Estate, Glasgow, Uk, G61 1QH

    Problematic publications fit publications listed here:

    https://www.gla.ac.uk/researchinstitutes/cancersciences/staff/maryscott/#publications

    Problematic publications Mary T Scott:-

    https://pubpeer.com/publications/237D18C38399F408830D40F3E21FD1

    https://pubpeer.com/publications/E3F5088239A7881A90C2CCE6762E56

    https://pubpeer.com/publications/A347AE5BB3D7D0A3828BB654F16D5A

    https://pubpeer.com/publications/8CE988307EBAA1F791A99AB678C107

    Like

  20. I bet Ted Hupp and Kathyryn Ball are morally outraged by “Partygate”, but what do they think they were doing?

    Like

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