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hyperresponsive promoter engaged the RelA:p52 dimer generated during costimulation of macrophages through TLR4 (show TLR4 Proteins) and LTbetaR to trigger synthesis of IkappaBalpha (show NFKBIA Proteins) at late time points, which prevented the late-acting RelA (show NFkBP65 Proteins) cross-talk response.
results suggest that changes in the relative concentrations of RelB (show RELB Proteins), NIK:IKK1, and p100 (show PATL2 Proteins) during noncanonical signaling modulate this transitional complex and are critical for maintaining the fine balance between the processing and protection of p100 (show PATL2 Proteins).
Results suggest that the RelB (show RELB Proteins)/NF-kappaB2 pathway regulates T cell migration to autoimmune targets in Sjogren syndrome through TGFbeta (show TGFB1 Proteins)/TGFbetaR-dependent regulation of CXCL12 (show CXCL12 Proteins)/CXCR4 (show CXCR4 Proteins) signaling.
MKK4 (show MAP2K4 Proteins) activates non-canonical NFkappaB signaling by promoting NFkappaB2-p100 (show PATL2 Proteins) processing.
the aberrant proliferative capacity of Brca1 (show BRCA1 Proteins)(-/-) luminal progenitor cells is linked to the replication-associated DNA damage response, where proliferation of mammary progenitors is perpetuated by damage-induced, autologous NF-kappaB (show NFKB1 Proteins) signaling.
RelB (show RELB Proteins) is processed by CO2 in a manner dependent on a key C-terminal domain located in its transactivation domain. Loss of the RelB (show RELB Proteins) transactivation domain alters NF-kappaB (show NFKB1 Proteins)-dependent transcriptional activity, and loss of p100 (show PATL2 Proteins) alters sensitivity of RelB (show RELB Proteins) to CO2
the individual functions of the NF-kappaB (show NFKB1 Proteins) family members NF-kappaB1 (show NFKB1 Proteins), NF-kappaB2 and c-REL (show NFkBP65 Proteins) in the various autoimmune pathologies of Fas(lpr/lpr (show FAS Proteins)) mutant mice, were investigated.
we identify in this study a critical role for the combined activity of the RELB (show RELB Proteins) and NF-kappaB2 subunits in B cell homeostasis that cannot be compensated for by the canonical NF-kappaB (show NFKB1 Proteins) pathway under physiological conditions.
Mechanistically the LncRNA-HIT siRNA treatments impacted pro-chondrogenic gene expression by reducing H3K27ac or p100 (show PATL2 Proteins) activity, confirming that LncRNA-HIT is essential for chondrogenic differentiation in the limb mesenchyme
Nfkb2 connected lymphotoxin (show LTB Proteins) signal within the intestinal niche in reinforcing epithelial innate inflammatory RelA (show NFkBP65 Proteins)/NF-kappaB (show NFKB1 Proteins) response to Citrobacter rodentium infection, while Nfkb2(-/-) mice succumbed to gut (show GUSB Proteins) infections owing to stromal defects.
NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF- kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF- kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. In a non-canonical activation pathway, the MAP3K14- activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes. The NF-kappa-B heterodimeric RelB-p52 complex is a transcriptional activator. The NF-kappa-B p52-p52 homodimer is a transcriptional repressor. NFKB2 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p100 and generation of p52 by a cotranslational processing. The proteasome-mediated process ensures the production of both p52 and p100 and preserves their independent function. p52 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. p52 and p100 are respectively the minor and major form\; the processing of p100 being relatively poor. Isoform p49 is a subunit of the NF-kappa-B protein complex, which stimulates the HIV enhancer in synergy with p65 (By similarity).
DNA-binding factor KBF2
, NF kappaB2
, nuclear factor NF-kappa-B p100 subunit
, nuclear factor of kappa light polypeptide gene enhancer in B-cells 2, p49/p100