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in vivo bioluminescence imaging in a transgenic model of inflammation showed that luciferase activity coincided with endogenous p52/p100 Nfkb2 expression
our studies for the first time establish p100 as a key tumor suppressor of bladder cancer growth
hyperresponsive promoter engaged the RelA:p52 dimer generated during costimulation of macrophages through TLR4 and LTbetaR to trigger synthesis of IkappaBalpha at late time points, which prevented the late-acting RelA cross-talk response.
results suggest that changes in the relative concentrations of RelB, NIK:IKK1, and p100 during noncanonical signaling modulate this transitional complex and are critical for maintaining the fine balance between the processing and protection of p100.
Results suggest that the RelB/NF-kappaB2 pathway regulates T cell migration to autoimmune targets in Sjogren syndrome through TGFbeta/TGFbetaR-dependent regulation of CXCL12/CXCR4 signaling.
MKK4 activates non-canonical NFkappaB signaling by promoting NFkappaB2-p100 processing.
the aberrant proliferative capacity of Brca1(-/-) 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 signaling.
RelB is processed by CO2 in a manner dependent on a key C-terminal domain located in its transactivation domain. Loss of the RelB transactivation domain alters NF-kappaB-dependent transcriptional activity, and loss of p100 alters sensitivity of RelB to CO2
the individual functions of the NF-kappaB family members NF-kappaB1, NF-kappaB2 and c-REL in the various autoimmune pathologies of Fas(lpr/lpr) mutant mice, were investigated.
we identify in this study a critical role for the combined activity of the RELB and NF-kappaB2 subunits in B cell homeostasis that cannot be compensated for by the canonical NF-kappaB pathway under physiological conditions.
Mechanistically the LncRNA-HIT siRNA treatments impacted pro-chondrogenic gene expression by reducing H3K27ac or p100 activity, confirming that LncRNA-HIT is essential for chondrogenic differentiation in the limb mesenchyme
Nfkb2 connected lymphotoxin signal within the intestinal niche in reinforcing epithelial innate inflammatory RelA/NF-kappaB response to Citrobacter rodentium infection, while Nfkb2(-/-) mice succumbed to gut infections owing to stromal defects.
Data indicate a coupled increase in the expression of renal, relA, NF-kB2, and p53 genes and proteins during folic acid induced acute kidney injury (AKI).
Loss of c-REL but not NF-kappaB2 prevents autoimmune disease driven by FasL mutation.
NF-kappaB2/p52 is necessary for the development of colitis, whilst c-Rel-mediated signalling regulates colonic epithelial cell turnover following DNA damage.
Nuclear translocation of c-Rel was enhanced in p100-deficient cells. p100, and not the processed p52 form, associated with c-Rel in the steady state and dissociated immediately after lipopolysaccharide stimulation in wild-type dendritic cells
The unique ability of p100/IkappaBdelta to stably interact with all NF-kappaB subunits by forming kappaBsomes demonstrates its importance in sequestering NF-kappaB subunits and releasing them as dictated by specific stimuli for developmental programs.
that p52 binds to the promoter of the GM-CSF-encoding gene (Csf2) and cooperates with c-Rel in the transactivation of this target gene.
NF-kappaB p65/p52 signaling mediated the effects of GDNF on Bcl-2 and Bcl-w expressions
NF-kappaB1- and NF-kappaB2-mediated signaling pathways differentially regulate the epithelial consequences of H. felis infection in the stomach.
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