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Article

All-trans retinoic acid induces p62DOK1 and p56DOK2 expression which enhances induced differentiation and G0 arrest of HL-60 leukemia cells.

American journal of hematology - 1 Aug 2006

Lamkin Thomas J, Chin Vivian, Yen Andrew

Abstract excerpt

p62(DOK1) (DOK1) and p56(DOK2) (DOK2) are sequence homologs that act as docking proteins downstream of receptor or nonreceptor tyrosine kinases. Originally identified in chronic myelogenous leukemia cells as a highly phosphorylated substrate for the chimeric p210(bcr-abl) protein, DOK1 was suspected to play a role in leukemogenesis. However, p62(DOK1-/-) fibroblast knockout cells were found to have enhanced MAPK...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression Regulation, Leukemic

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Source

Identifiers

PMID: 16823827
DOI: 10.1002/ajh.20667

Genes

DOK1
DOK2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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All-trans retinoic acid induces p62DOK1 and p56DOK2 expression which enhances induced differentiation and G0 arrest of HL-60 leukemia cells.PMID 16823827Read ↗

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retinoic acid, bromodeoxyuridine, and the Delta 205 mutant polyoma virus middle T antigen regulate expression levels of a common ensemble of proteins associated with early stages of inducing HL-60 leukemic cell differentiation.Semantic proximity Read ↗

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