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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to MBD2

HDAC1 — MBD2

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Schutyser et al., J Immunol 2000 (Cell Transformation, Neoplastic) : Although coinduced with monocyte chemotactic protein-1 (MCP-1) and IL-8 by dsRNA, measles virus, and IL-1beta in diploid fibroblasts, leukocytes produced LARC/MIP-3alpha only in response to LPS
Sekimata et al., J Biol Chem 2001 : This repression is attenuated by an HDAC inhibitor, trichostatin A, and is completely dependent on the interaction with MBD2
Cardoso et al., Dev Biol 2005 : This study thus demonstrates that in vivo XNP-1 acts in association with RB, HP1 and the NuRD complex during development
Yoshikawa et al., Arch Otolaryngol Head Neck Surg 2006 (Cholesteatoma, Middle Ear) : The messenger RNA expressions of LARC ( liver and activation regulated chemokine ), GMCSF ( granulocyte-macrophage colony stimulating factor ), epiregulin, ICAM1 ( intercellular adhesion molecule 1 ), and TGFA ( transforming growth factor alpha ) were more strongly up-regulated by IL-1alpha and/or IL-1beta in MECF than in SF, suggesting that these fibroblasts derived from different tissues retained their typical gene expression profiles ... The messenger RNA expressions of LARC ( liver and activation regulated chemokine ), GMCSF ( granulocyte-macrophage colony stimulating factor ), epiregulin, ICAM1 ( intercellular adhesion molecule 1 ), and TGFA ( transforming growth factor alpha ) were more strongly up-regulated by IL-1alpha and/or IL-1beta in MECF than in SF, suggesting that these fibroblasts derived from different tissues retained their typical gene expression profiles
Topark-Ngarm et al., J Biol Chem 2006 (Neuroblastoma) : Therefore, it seems likely that the NuRD complex may be involved in transcriptional repression of CTIP2 target genes and contribute to the function ( s ) of CTIP2 within a neuronal context
Gopal et al., Cell cycle (Georgetown, Tex.) 2006 (Inflammation) : The resulting depletion of cellular HDAC1 levels lead to a consequent depletion of HDAC1 associated with the CDKN1A gene promoter and increased expression of its protein product, p21 ( WAF1/CIP1 )