The p65 (RelA) Subunit of NF-κB Interacts with the Histone Deacetylase (HDAC) Corepressors HDAC1 and HDAC2 To Negatively Regulate Gene Expression

By B. P. Ashburner, S. Westerheide, A. Baldwin. Molecular and Cellular Biology, 2001

781 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4eb098afd7a6992e7a85aeafae9e4278027fa725

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Citations in the corpus

Modulation of NF‐κB‐dependent transcription and cell survival by the SIRT1 deacetylase (2004, background): “HDAC1, HDAC2, and HDAC3 deacetylate RelA/p65, resulting in increased IkBa association or loss of transactivation potential of the protein (Ashburner et al, 2001; Chen et al, 2001; Zhong et al, 2002).”
The complexity of NF-κB signaling in inflammation and cancer (2013, background): “Besides the very well defined interactions between the various members of the NF-κB family, and the interactions with their inhibitors such as IκBα, IκBβ or IκBε [46-49], NF-κB molecules have been shown to interact with upstream kinases, with chromatinmodifiers such as histone deacetylases (HDACs), ”
A Nurr1/CoREST transrepression pathway attenuates neurotoxic inflammation in activated microglia and astrocytes (2009, neutral): “Error bars represent the SD. scription ( Ashburner et al., 2001 ).”
The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression. (2003, background): “Besides HDAC-2, association of NF- B with HDAC-1 and HDAC-3 has also been observed recently (77, 467, 468).”
EMT, cancer stem cells and drug resistance: an emerging axis of evil in the war on cancer (2010, background): “Furthermore, HDACs can affect the activity of nonhistone substrates, such as HIF-1 (Jeong et al., 2002; Kong et al., 2006) and nuclear factor-kB (Ashburner et al., 2001), which have been implicated in driving EMT and drug resistance.”
Modulation of NF-κB Activity by Exchange of Dimers (2003, background): “Paralleling the activa- histone-modifying enzymes have been shown to interact tion of the two pathways, a sequential recruitment of with NF- B proteins (Ashburner et al., 2001; Barboric et dimers was observed.”
IκBα and p65 Regulate the Cytoplasmic Shuttling of Nuclear Corepressors: Cross-talk between Notch and NFκB Pathways (2003, background): “Because different corepressor complexes interact with NF B (Lee et al., 2000; Ashburner et al., 2001; Baek et al., 2002) and other transcription factors (Bailey et al., 1999; Wu et al., 2001; Melnick et al., 2000), we are currently examining the composition of the putative complex that may…”