World's Best Scientists 2026 revealed!

D-Index & Metrics

Biology and Biochemistry

D-Index
47
Citations
8933
World Ranking
18669
National Ranking
1456

Overview

Martin J. Allday is affiliated with Imperial College London in the United Kingdom. Their work is connected to this institution, reflecting an involvement in the academic environment of one of the leading research universities.

There is no available data regarding recent papers authored by Martin J. Allday or frequent coauthors linked with their research. Similarly, details about the venues where they regularly publish are not provided, nor are there records of book publications associated with their name.

Information about the main fields of study, subfields, or primary research topics covered by Martin J. Allday is also not available. Additionally, there is no record of awards won or distinctions received by this researcher documented in the data provided.

Best Publications

  • A common polymorphism acts as an intragenic modifier of mutant p53 behaviour

    Maria Carmen Marin;Christine A. Jost;Louise A. Brooks;Meredith S. Irwin

  • The curious case of the tumour virus: 50 years of Burkitt's lymphoma

    David A. Thorley-Lawson;Martin J. Allday

  • A degradation signal located in the C‐terminus of p21WAF1/CIP1 is a binding site for the C8 α‐subunit of the 20S proteasome

    Robert Touitou;Jo Richardson;Suchira Bose;Makoto Nakanishi

  • EBV gene expression in an NPC-related tumour.

    M.M. Hitt;M.J. Allday;T. Hara;L. Karran

  • MDM2 Promotes Proteasome-Dependent Ubiquitin-Independent Degradation of Retinoblastoma Protein

    Patima Sdek;Haoqiang Ying;Donny L.F. Chang;Wei Qiu

  • Genome Diversity of Epstein-Barr Virus from Multiple Tumor Types and Normal Infection

    Anne L. Palser;Nicholas E. Grayson;Robert E. White;Craig Corton

  • Epigenetic reprogramming of host genes in viral and microbial pathogenesis

    Konstantinos Paschos;Martin J. Allday

  • High level expression of ΔN-p63: a mechanism for the inactivation of p53 in undifferentiated nasopharyngeal carcinoma (NPC)?

    Tim Crook;John M Nicholls;Louise Brooks;Jenny O'Nions

  • An ATM/Chk2-Mediated DNA Damage-Responsive Signaling Pathway Suppresses Epstein-Barr Virus Transformation of Primary Human B Cells

    Pavel A. Nikitin;Christopher M. Yan;Eleonora Forte;Alessio Bocedi

  • Two Epstein-Barr virus (EBV) oncoproteins cooperate to repress expression of the proapoptotic tumour-suppressor Bim: clues to the pathogenesis of Burkitt's lymphoma.

    E Anderton;J Yee;P Smith;T Crook

  • Immunohistology of Epstein-Barr virus-associated antigens in B cell disorders from immunocompromised individuals.

    J. Thomas;Neil Hotchin;Martin Allday;Peter Amlot

  • p53 mutation with frequent novel codons but not a mutator phenotype in BRCA1- and BRCA2-associated breast tumours

    Tim Crook;Louise A Brooks;Susan Crossland;P Osin

  • Epstein-Barr Virus Nuclear Antigen 3C Interacts with Histone Deacetylase To Repress Transcription

    Stoyan A Radkov;Robert Touitou;Alex Brehm;Martin Rowe

  • Epstein-barr virus latency in B cells leads to epigenetic repression and CpG methylation of the tumour suppressor gene Bim.

    Kostas Paschos;Paul Smith;Emma Anderton;Jaap M. Middeldorp

  • Epstein-Barr virus nuclear antigen (EBNA)3C is an immortalizing oncoprotein with similar properties to adenovirus E1A and papillomavirus E7.

    G A Parker;T Crook;M Bain;E A Sara

  • EBNA3B-deficient EBV promotes B cell lymphomagenesis in humanized mice and is found in human tumors

    Robert E. White;Patrick C. Rämer;Kikkeri N. Naresh;Sonja Meixlsperger

  • Epigenetic Repression of p16INK4A by Latent Epstein-Barr Virus Requires the Interaction of EBNA3A and EBNA3C with CtBP

    Lenka Skalska;Robert E. White;Melanie Franz;Michaela Ruhmann

  • Epstein-Barr virus latent gene expression during the initiation of B cell immortalization.

    M. J. Allday;D. H. Crawford;B. E. Griffin

  • Interaction of MEQ protein and C-terminal-binding protein is critical for induction of lymphomas by Marek's disease virus

    Andrew C. Brown;Susan J. Baigent;Lorraine P. Smith;Jason P. Chattoo

  • Transcriptional silencing of Polo-like kinase 2 (SNK/PLK2) is a frequent event in B-cell malignancies.

    Nelofer Syed;Paul Smith;Alexandra Sullivan;Lindsay C Spender

Frequent Co-Authors

Paul J. Farrell
Paul J. Farrell Imperial College London
Paul D. Smith
Paul D. Smith AstraZeneca (United Kingdom)
Beverly E. Griffin
Beverly E. Griffin Imperial College London
Venugopal Nair
Venugopal Nair The Pirbright Institute
Christian Münz
Christian Münz University of Zurich
Jaap M. Middeldorp
Jaap M. Middeldorp VU University Medical Center
David A. Thorley-Lawson
David A. Thorley-Lawson Tufts University
Anthony Letai
Anthony Letai Harvard University
Paul Kellam
Paul Kellam Imperial College London
Gerald Niedobitek
Gerald Niedobitek University of Erlangen-Nuremberg

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