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Peter D. Adams

Researcher at University of Glasgow

Publications -  128
Citations -  20807

Peter D. Adams is an academic researcher from University of Glasgow. The author has contributed to research in topics: Senescence & Chromatin. The author has an hindex of 54, co-authored 115 publications receiving 17101 citations. Previous affiliations of Peter D. Adams include Discovery Institute & Fox Chase Cancer Center.

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Retinoblastoma protein contains a C-terminal motif that targets it for phosphorylation by cyclin-cdk complexes.

TL;DR: The C terminus of pRB contains a cyclin-cdk interaction motif of the type found in E2F1 and p21 that enables it to be recognized and phosphorylated by cyclin -cdk complexes.
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Remodeling of chromatin structure in senescent cells and its potential impact on tumor suppression and aging.

TL;DR: The current understanding of the structure, assembly and function of these Senescence-Associated Heterochromatin Foci at a cellular level is reviewed.
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Structure of a human ASF1a-HIRA complex and insights into specificity of histone chaperone complex assembly.

TL;DR: The crystal structure of an ASF1a–HIRA heterodimer and a biochemical dissection of ASF 1a's mutually exclusive interactions with HIRA and the p60 subunit of CAF-1 begin to define the molecular determinants of assembly of functionally diverse macromolecular histone chaperone complexes.
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Coupling of DNA Synthesis and Histone Synthesis in S Phase Independent of Cyclin/cdk2 Activity

TL;DR: It is shown that ectopic expression of HIRA, the likely human ortholog of two cell cycle-regulated repressors of histone gene transcription in yeast, represses transcription of histones and that this, in turn, triggers a concerted block of DNA synthesis.
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Definition of pRB- and p53-Dependent and -Independent Steps in HIRA/ASF1a-Mediated Formation of Senescence-Associated Heterochromatin Foci

TL;DR: Evidence indicates that downstream of HIRA's localization to PML bodies, the HIRA/ASF1a pathway cooperates with pRB and p53 to make SAHF, with the HI RA/ASf1a and pRB pathways acting in parallel.