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

◀ Back to NFKB1

HDAC2 — NFKB1

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

Xiao et al., J Biol Chem 2000 : Consistently, when expressed alone, the NRD potently inhibits NIK mediated NF-kappaB signaling
Ashburner et al., Mol Cell Biol 2001 : HDAC2 does not interact with NF-kappaB directly but can regulate NF-kappaB activity through its association with HDAC1
Rahman et al., Biochem Pharmacol 2002 (Pneumonia) : Pharmacological inhibition of HDAC leads to the increased HAT activity, AP-1 and NF-kappaB activation, and IL-8 release by H2O2 or TNF-alpha treatments
Mayo et al., J Biol Chem 2003 (Carcinoma, Non-Small-Cell Lung...) : Because the anti-apoptotic transcription factor NF-kappa B has been shown to be under the control of HDAC mediated repression, we analyzed whether HDAC inhibitors activated NF-kappa B in NSCLC cells ... HDAC inhibitors effectively stimulated endogenous NF-kappa B-dependent gene expression by up-regulating IL-8, Bcl-XL, and MMP-9 transcripts
Foss et al., Leukemia & lymphoma 2003 (Lymphoma, T-Cell, Cutaneous) : Other novel agents include the interleukin (IL)-2 fusion toxin ( ONTAK ), pentostatin ( a potent adenosine deaminase inhibitor ), histone deacetylase inhibitors such as depsipeptide, NF-kappaB inhibitors , cytokine receptor antagonists, immunomodulatory therapies and allogeneic stem cell therapy
Singh et al., Oncogene 2005 (Breast Neoplasms) : HDAC inhibitors synergized with TRAIL by inducing DRs DR4/TRAIL-R1 and DR5/TRAIL-R2 through NFkappaB activation and some of the proapoptotic members of the Bcl-2 family, and engaging the mitochondrial pathway
Place et al., Biochem Pharmacol 2005 : HDAC inhibition prevents NF-kappa B activation by suppressing proteasome activity : down-regulation of proteasome subunit expression stabilizes I kappa B alpha
Shetty et al., Mol Cell Biol 2005 (Breast Neoplasms) : Indeed, HDAC inhibitors activate NF-kappaB and p53 and upregulate DR5 expression
Graham et al., Cell cycle (Georgetown, Tex.) 2005 : In addition, HDAC inhibitors induce NFkappaB binding to the DR5 gene and DR5 expression, contributing to HDAC inhibitor induced apoptosis
Ito et al., J Exp Med 2006 (Pulmonary Disease, Chronic Obstructive) : Loss of HDAC2 did not reduce GR nuclear translocation, GR binding to glucocorticoid response element ( GRE ) on DNA, or GR-induced DNA or gene induction but inhibited the association between GR and NF-kappaB
Kammanadiminti et al., J Biol Chem 2006 (Colitis) : Overexpression of wild type Hsp27 amplified the effects of SAP, whereas a phosphorylation-deficient mutant of Hsp27 abrogated SAP induced NF-kappaB inhibition
Kim et al., Biochem Biophys Res Commun 2006 : Involvement of HDAC1 and the PI3K/PKC signaling pathways in NF-kappaB activation by the HDAC inhibitor apicidin ... Furthermore, apicidin activation of NF-kappaB seems to result from HDAC1 inhibition, as evidenced by the observation that overexpression of HDAC1, but not HDAC2 , 3 or 4, dramatically inhibits NF-kappaB reporter gene activity
Andresen et al., J Immunol 2007 : NF-kappaB activity can be induced by HDAC treatment
Glauben et al., Gut 2008 (Colitis...) : As for potential mechanisms of ITF2357 action, increased acetylation of histone 3, reduced production of IFN gamma and enhanced apoptosis in lamina propria mononuclear cells were found to accompany a histone deacetylase dependent activation of NF-kappaB
Kaler et al., Exp Cell Res 2008 (Colonic Neoplasms) : We showed that overexpression of HDAC2 enhanced TNFalpha induced NF-kappaB activity and that silencing of HDAC2 decreased NF-kappaB activity
Hayes et al., Eur J Nutr 2008 (Neoplasms) : In particular, their abilities to induce cytoprotective genes, mediated by the Nrf2 ( NF-E2 related factor 2 ) and AhR ( arylhydrocarbon receptor ) transcription factors, and their abilities to repress NF-kappaB ( nuclear factor-kappaB ) activity, inhibit histone deacetylase , and inhibit cytochrome P450 are outlined
Chavey et al., Mol Pharmacol 2008 (Breast Neoplasms) : In summary, our results demonstrate that NF-kappaB pathway repression by HDAC is responsible for the low expression of IL-8 in ERalpha positive breast cancer cells
Farhana et al., Mol Cancer Ther 2009 : We examined the effect of loss of SHP and Sin3A expression in a number of cell types on 3-Cl-AHPC mediated growth inhibition and apoptosis induction, 3-Cl-AHPC mediated nuclear factor-kappaB (NF-kappaB) activation, and 3-Cl-AHPC mediated increase in c-Fos and c-Jun expression
Zhang et al., Am J Physiol Heart Circ Physiol 2010 (Disease Models, Animal...) : Luciferase assay demonstrated an activation of NF-kappaB by HDAC inhibition