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Recombination signal binding protein for immunoglobulin kappa J region

CBF1, RBP-Jkappa, RBP-J
The protein encoded by this gene is a transcriptional regulator important in the Notch signaling pathway. The encoded protein acts as a repressor when not bound to Notch proteins and an activator when bound to Notch proteins. It is thought to function by recruiting chromatin remodeling complexes containing histone deacetylase or histone acetylase proteins to Notch signaling pathway genes. Also, this protein can bind specifically to the recombination signal sequence of immunglobulin kappa type J segments. Several transcript variants encoding different isoforms have been found for this gene, and several pseudogenes of this gene exist on chromosome 9. [provided by RefSeq, Oct 2011] (from NCBI)
Top mentioned proteins: RBP, p300, CAN, FATE, Barr
Papers on CBF1
Forced Activation of Notch in Macrophages Represses Tumor Growth by Upregulating miR-125a and Disabling Tumor-Associated Macrophages.
Qin et al., Key West, United States. In Cancer Res, Feb 2016
Macrophage miRNA profiling identified a novel downstream mediator of Notch signaling, miR-125a, which was upregulated through an RBP-J-binding site at the first intronic enhancer of the host gene Spaca6A.
EBNA3C Directs Recruitment of RBPJ (CBF1) to Chromatin during the Process of Gene Repression in EBV Infected B Cells.
Allday et al., London, United Kingdom. In Plos Pathog, Jan 2016
Most remarkable, and in contrast to current models of RBPJ in repression, was the observation that this DNA-binding factor accumulated at the EBNA3C-binding sites only when EBNA3C was functional.
Search for regulatory factors of the pituitary-specific transcription factor PROP1 gene.
Kato et al., Japan. In J Reprod Dev, Jan 2016
Their regulatory factors, except for RBP-J, have not yet been clarified.
The DEAD-Box RNA Helicase AtRH7/PRH75 Participates in Pre-rRNA Processing, Plant Development and Cold Tolerance in Arabidopsis.
Lu et al., Taiwan. In Plant Cell Physiol, Jan 2016
In addition, the atrh7-2 and atrh7-3 mutants displayed cold hypersensitivity and decreased expression of CBF1, CBF2 and CBF3, which might be responsible for the cold intolerance.
[Effects of exogenous EBR and NO signal on antioxidant system and low response gene expression under cold stress on maize embryo].
Du et al., In Ying Yong Sheng Tai Xue Bao, May 2015
The gene expression pattern analysis showed that the expression of P5CS1, CBF1, CBF3 and COR15a was induced by LT stress, and further increased by EBR treatment in maize embryo, while their expression was suppressed by c-PTIO and L-NAME, and improved by SNP, which implied LT-responsed genes were regulated by NO.
The role of epigenetic mechanisms in Notch signaling during development.
Schwanbeck, Kiel, Germany. In J Cell Physiol, May 2015
There it binds to the Notch effector protein RBP-J, displaces a corepressor complex and enables the induction of target genes by recruitment of coactivators in a cell-context dependent manner.
NF-κB-Mediated Regulation of Osteoclastogenesis.
Yao et al., Rochester, United States. In Endocrinol Metab (seoul), Apr 2015
However, these cytokines also activate NF-κB signaling that can limit osteoclast formation through the NF-κB signaling proteins, TRAF3 and p100, and the suppressors of c-Fos/NFATc1 signaling, IRF8, and RBP-J.
The multifaceted role of the embryonic gene Cripto-1 in cancer, stem cells and epithelial-mesenchymal transition.
Salomon et al., Frederick, United States. In Semin Cancer Biol, 2014
Finally, CR-1 can facilitate signaling through the canonical Wnt/β-catenin and Notch/Cbf-1 pathways by functioning as a chaperone protein for LRP5/6 and Notch, respectively.
Fate and plasticity of renin precursors in development and disease.
Sequeira-Lopez et al., Charlottesville, United States. In Pediatr Nephrol, 2014
Notably, key transcriptional (Creb/CBP/p300, RBP-J) and posttranscriptional (miR-330, miR125b-5p) effectors of those signaling pathways are prominent in the regulation of renin cell identity.
[Analysis on signaling pathway network of proliferation of neural stem cells].
Li et al., In Zhongguo Zhong Yao Za Zhi, 2014
With the Notch pathway as the core of the network, this paper summarized the advance of the bimolecular network system composed of Wnt, Shh, EGFR, cytokines and Notch signal, and analyzed such key nodes as Notch receptor, CBF1, NICD, Hesl, which may become potential targets of new-type drugs in the future.
Notch and TGFβ form a reciprocal positive regulatory loop that suppresses murine prostate basal stem/progenitor cell activity.
Xin et al., Houston, United States. In Cell Stem Cell, 2012
Disrupting the canonical Notch effector Rbp-j impairs the differentiation of prostate basal stem cells and increases their proliferation in vitro and in vivo, but does not affect luminal cell biology.
RBPJ mutations identified in two families affected by Adams-Oliver syndrome.
Gaffney et al., Oklahoma City, United States. In Am J Hum Genet, 2012
Unique mutations in RBPJ lead to impaired DNA binding in cases of Adams-Oliver syndrome.
Notch-RBP-J signaling regulates the transcription factor IRF8 to promote inflammatory macrophage polarization.
Hu et al., New York City, United States. In Nat Immunol, 2012
The results defined a signaling network in which signaling via Notch-RBP-J and TLRs is integrated at the level of IRF8 synthesis. A mechanism was identified by which heterologous signaling pathways can regulate TLR-induced polarization of macrophages.
Multifocal epithelial tumors and field cancerization from loss of mesenchymal CSL signaling.
Dotto et al., Lausanne, Switzerland. In Cell, 2012
Mice carrying a mesenchymal-specific deletion of CSL/RBP-Jkappa, a key Notch effector, exhibit spontaneous multifocal keratinocyte tumors that develop after dermal atrophy and inflammation.
Notch-mediated patterning and cell fate allocation of pancreatic progenitor cells.
Jensen et al., Cleveland, United States. In Development, 2012
Data found direct binding of RBP-jkappa to the Nkx6.1 proximal promoter.
Physiological notch signaling maintains bone homeostasis via RBPjk and Hey upstream of NFATc1.
Long et al., Saint Louis, United States. In Plos Genet, 2011
Notch-RBPjk signaling functions in part through Hey1-mediated inhibition of NFATc1 to suppress osteoblastogenesis, contributing to bone homeostasis in vivo
Quiescent and active hippocampal neural stem cells with distinct morphologies respond selectively to physiological and pathological stimuli and aging.
Giachino et al., Freiburg, Germany. In Cell Stem Cell, 2010
We show that canonical Notch signaling through RBP-J is required for hippocampal neurogenesis.
Nemo-like kinase suppresses Notch signalling by interfering with formation of the Notch active transcriptional complex.
Itoh et al., Nagoya, Japan. In Nat Cell Biol, 2010
High levels of Notch-mediated transcriptional activation require the formation of a ternary complex consisting of NotchICD, CSL (CBF-1, suppressor of hairless, LAG-1) and a Mastermind family member.
Integrated regulation of Toll-like receptor responses by Notch and interferon-gamma pathways.
Ivashkiv et al., New York City, United States. In Immunity, 2008
Cooperation by these pathways to increase target gene expression was mediated by the Notch-pathway component and transcription factor RBP-J, which also contributed to lethality after endotoxin injection.
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