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Human Polyclonal RELB Primary Antibody for IHC - ABIN966960
Pyz, Naidenko, Miyake, Yamamura, Berberich, Cardell, Kronenberg, Herrmann: The complementarity determining region 2 of BV8S2 (V beta 8.2) contributes to antigen recognition by rat invariant NKT cell TCR. in Journal of immunology (Baltimore, Md. : 1950) 2006
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Human RELB Primary Antibody for IHC - ABIN966959
Marienfeld, Berberich-Siebelt, Berberich, Denk, Serfling, Neumann: Signal-specific and phosphorylation-dependent RelB degradation: a potential mechanism of NF-kappaB control. in Oncogene 2002
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Human Polyclonal RELB Primary Antibody for IF (p), IHC (p) - ABIN700825
Ta, Schwensen, Liuwantara, Huso, Watnick, Rangan: Constitutive renal Rel/nuclear factor-κB expression in Lewis polycystic kidney disease rats. in World journal of nephrology 2016
Study findings demonstrate that RelB, involved in noncanonical NF-kappaB signaling, is upregulated by TRAF2 and is required for mediating the cytoprotective effects of TRAF2 overexpression in mouse model of myocardial infarction. Cytoprotective effects of TRAF2 are mediated by crosstalk between the canonical and noncanonical NF-kappaB signaling pathways, thereby revealing a complexity for NF-kappaB signaling in the heart.
RELB is required for the ductular reaction and development of biliary fibrosis in CyldDLPC mice. Deletion of RELB and CYLD from LPCs protects mice from DDCinduced cholestatic liver fibrosis.
the autoimmune phenotype in germline RelB-deficient mice is most likely caused by T cell-extrinsic mechanisms
these results show that RelB in dendritic cells is important for Th2 induction by regulating the development of CD117+CD172a+ dendritic cells and for the priming of allergic pulmonary hyperreactions
Results indicate an epithelial intrinsic role of transcription factor RelB (RelB) on medullary thymic epithelial cells (mTECs) development and function.
Eda-activated RelB recruits BAF complex to specific gene loci for local chromatin remodeling of target genes.
this study shows that RelB regulates Th17 differentiation in a cell-intrinsic manner
The data indicate that RelB deficiency may be a key pathway underlying allergic airway inflammation, and that dendritic cell-encoded RelB is sufficient to restore control of this inflammation.
RelB role in the dendritic and myeloid cells development
these data support that RelB suppresses cigarette smoke-induced apoptosis, potentially by increasing the AhR
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.
CCR7 overexpression and RelB knockdown (KD) in imDCs improve skin-graft survival in a murine skin-transplantation model. Transfection with Ad-CCR7 and RelB KD in imDCs may be an effective approach inducing immune tolerance, thus being potentially valuable for inhibiting allograft rejection.
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
this study shows that RelB-silencing in dendritic cells generates dendritic cells of tolerogenic properties with immunomodulatory function and appears as potential option of cell-targeted therapy
AhR and NF-kappaB/Rel protein binding profile within the 3'IghRR mediates the inhibitory effects of TCDD on Ig expression and therefore antibody levels.
Relb is necessary for the effective production of downstream RANK(+) medullary thymic epithelial cell progenitors.
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.
results indicate that BAFF signals coordinate both RelB and cRel activities to ensure survival during peripheral B-cell maturation
phosphorylation of DBC1 at its C terminus by IKKalpha facilitates its interaction with RelB and IKKalpha, indicating that DBC1-mediated suppression of alternative NF-kappaB is regulated by IKKalpha.
In human liver diseases, RELB is upregulated in cholangiocytes. Activation of non-canonical NF-kB subunit RELB drives ductular reaction, oval cell activation and biliary driven fibrosis.
Expression of RelB by cells of colorectal cancer patients is associated with poor survival
Results show that GSK3beta modulates RelB degradation.
The riboflavin transporter-3 (SLC52A3) 5'-flanking regions contain NF-kappaB p65/Rel-B-binding sites, which are crucial for mediating SLC52A3 transcriptional activity in esophageal squamous cell carcinoma (ESCC) cells.
Data show that TNF receptor-associated factor 3 (TRAF3) autophagy is driven by RAS and results in activation of transcription factor RelB (RELB).
TNF-alpha-induced expression of transport protein genes in HUVEC cells is associated with enhanced expression of RELB and NFKB2.
Low RELB expression is associated with Prostate Cancer.
NF-kappaB RelB protein, but not RelA, displayed high expression in Endometrial cancer samples and cell lines.
to elucidate the induced activation of lytic pathway by ionizing radiation, irradiated SNU-719 cells were checked for the RelA and RelB expression by real-time PCR. RelB level showed a dose-dependent enhancement on 2nd and 4th day, whereas only a slight upregulation in RelA is noticed
EZH2, through a methyltransferase-independent mechanism, promotes the transcriptional activation of the non-canonical NF-kappaB subunit RelB
The altered expression of anti-apoptotic gene Bcl-2 played critical roles in regulating both spontaneous and radiation-induced apoptosis in the presence of RelB knockdown. For the first time, we showed that RelB knockdown significantly attenuated the migration and invasion of DU145 prostate cancer cells, due to the reduction of integrin b-1
Knockdown of ADGRG2 breast cancer cell lines resulted in a strong reduction in cell adhesion and subsequent cell migration which was associated with a selective reduction in RelB.
the role of RelB on lymphocyte development in humans was shown.
In conclusion, DECs show a unique hypo-responsive phenotype to the pro-inflammatory stimulus LPS in order to control the inflammatory response at feto-maternal interface.
Lung-specific (CC-16) and novel (RelB) biomarkers are associated with systemic cardiovascular changes over time.
results suggest that glucocorticoids induce a transcription complex consisting of RelB/p52, CBP, and HDAC1 that triggers a dynamic acetylation-mediated epigenetic change to induce CRH expression in full-term human placenta.
HDAC4-RelB-p52 complex maintains repressive chromatin around proapoptotic genes Bim and BMF and regulates multiple myeloma survival and growth
RELB enhances proliferation of human-induced pluripotent stem cells without affecting their pluripotency. RELB interacts with LIN28A and IMP3.
Bovine foamy virus transactivator BTas interacts with cellular RelB to enhance viral transcription.
XRelB can partially substitute for several, but not all, functions of the Dorsal protein in Drosophila embryos.
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. NF-kappa-B heterodimeric RelB-p50 and RelB-p52 complexes are transcriptional activators. Stimulates promoter activity in the presence of p49- and p50-NF-kappa-B. Neither associates with DNA nor with p65-NF-kappa-B (By similarity).
transcription factor RelB
, v-rel avian reticuloendotheliosis viral oncogene homolog B (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3)
, v-rel reticuloendotheliosis viral oncogene homolog B, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3
, avian reticuloendotheliosis viral (v-rel) oncogene related B
, v-rel reticuloendotheliosis viral oncogene homolog B
, transcription factor RelB homolog