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Recombinant Mouse Recombining binding protein suppressor of hairless (Rbpj)

  • 货号:
    CSB-YP019486MO
  • 规格:
  • 来源:
    Yeast
  • 其他:
  • 货号:
    CSB-EP019486MO
  • 规格:
  • 来源:
    E.coli
  • 其他:
  • 货号:
    CSB-EP019486MO-B
  • 规格:
  • 来源:
    E.coli
  • 共轭:
    Avi-tag Biotinylated

    E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.

  • 其他:
  • 货号:
    CSB-BP019486MO
  • 规格:
  • 来源:
    Baculovirus
  • 其他:
  • 货号:
    CSB-MP019486MO
  • 规格:
  • 来源:
    Mammalian cell
  • 其他:

产品详情

  • 纯度:
    >85% (SDS-PAGE)
  • 基因名:
  • Uniprot No.:
  • 别名:
    Rbpj; Igkjrb1; Igkrsbp; Rbpsuh; Recombining binding protein suppressor of hairless; J kappa-recombination signal-binding protein; RBP-J kappa
  • 种属:
    Mus musculus (Mouse)
  • 蛋白长度:
    Full length protein
  • 表达区域:
    1-526
  • 氨基酸序列
    MPSGFPQSPR TSPRARPKTR ITGALPMDYS EGLSAEERPA HAPSAGKFGE RPPPKRLTRE AMRNYLKERG DQTVLILHAK VAQKSYGNEK RFFCPPPCVY LMGSGWKKKK EQMERDGCSE QESQPCAFIG IGNSDQEMQQ LNLEGKNYCT AKTLYISDSD KRKHFMLSVK MFYGNSDDIG VFLSKRIKVI SKPSKKKQSL KNADLCIASG TKVALFNRLR SQTVSTRYLH VEGGNFHASS QQWGAFYIHL LDDDESEGEE FTVRDGYIHY GQTVKLVCSV TGMALPRLII RKVDKQTALL DADDPVSQLH KCAFYLKDTE RMYLCLSQER IIQFQATPCP KEQNKEMIND GASWTIISTD KAEYTFYEGM GPVLAPVTPV PVVESLQLNG GGDVAMLELT GQNFTPNLRV WFGDVEAETM YRCGESMLCV VPDISAFREG WRWVRQPVQV PVTLVRNDGV IYSTSLTFTY TPEPGPRPHC SAAGAILRAN SSQVPSNESN TNSEGNYTNA STNSTSVTSS TATVVS
  • 蛋白标签:
    Tag type will be determined during the manufacturing process.
    The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
  • 产品提供形式:
    Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 复溶:
    We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
  • 储存条件:
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保质期:
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 货期:
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事项:
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet :
    Please contact us to get it.

产品评价

靶点详情

  • 功能:
    Transcriptional regulator that plays a central role in Notch signaling, a signaling pathway involved in cell-cell communication that regulates a broad spectrum of cell-fate determinations. Acts as a transcriptional repressor when it is not associated with Notch proteins. When associated with some NICD product of Notch proteins (Notch intracellular domain), it acts as a transcriptional activator that activates transcription of Notch target genes. Probably represses or activates transcription via the recruitment of chromatin remodeling complexes containing histone deacetylase or histone acetylase proteins, respectively. Specifically binds to the immunoglobulin kappa-type J segment recombination signal sequence. Binds specifically to methylated DNA. Binds to the oxygen responsive element of COX4I2 and activates its transcription under hypoxia conditions (4% oxygen). Negatively regulates the phagocyte oxidative burst in response to bacterial infection by repressing transcription of NADPH oxidase subunits.
  • 基因功能参考文献:
    1. homoeostatic repressor of multiple pro-angiogenic and angiostatic factor genes in cardiomyocytes PMID: 27357444
    2. Early pancreatic islet fate and maturation is controlled through RBP-Jkappa. PMID: 27240887
    3. In this study, the s found that conditional disruption of RBP-J, the transcription factor of canonical Notch signaling, increased irradiation sensitivity in mice. PMID: 27188577
    4. Macrophage maturation is controlled by Notch ligand Dll1 expressed in vascular endothelial cells of arteries and requires macrophage canonical Notch signaling via Rbpj, which simultaneously suppresses an inflammatory macrophage fate. Conversely, conditional mutant mice lacking Dll1 or Rbpj show proliferation and transient accumulation of inflammatory macrophages, which antagonizes arteriogenesis and tissue repair. PMID: 29038527
    5. RBPJ binds and trans-activates the Il23r promoter and induces IL-23R expression and represses anti-inflammatory IL-10 production in Th17 cells. PMID: 27346359
    6. RBP-J deficiency drastically reduced dopamine release in the striatum and caused a subtle decrease in the number of dopaminergic neurons. These findings demonstrated that Notch/RBP-J signaling regulates dopamine responsiveness in the striatum, which may explain the mechanism whereby Notch/RBP-J signaling affects an individual's susceptibility to neuropsychiatric disease. PMID: 28267151
    7. RBP-J-mediated Notch signalling is critical for basophil-dependent immunoregulation. Deficiency of RBP-J influences the immunoregulatory functions of BA, which include activation of T cells and their differentiation into T helper cell subtypes. PMID: 28493549
    8. study uncovered a regulatory network, where miR-182 functions as an important new node that receives inputs from RBP-J and TNF-alpha signaling and positively regulates inflammatory osteoclastogenesis; suppression of miR-182 by RBP-J serves as an important mechanism that restrains TNF-alpha induced osteoclastogenesis PMID: 27183593
    9. structural and biophysical studies demonstrate that RITA binds RBP-J similarly to the RAM (RBP-J-associated molecule) domain of Notch, our biochemical and cellular assays suggest that RITA interacts with additional regions in RBP-J. PMID: 28487372
    10. RBP-J mediated by miR-133a probably contributed to the regulation of DCs maturation and activation in osteosarcoma PMID: 27794430
    11. Rbpj-kappa mediated Notch signaling plays a critical role in development of hypothalamic Kisspeptin neurons. PMID: 26318021
    12. Results reveal an essential role for canonical Notch/RBP-J signaling in hippocampal synaptic plasticity and suggest that role, at least in part, is mediated by the regulation of GABAergic signaling PMID: 25515406
    13. The bone marrow contains a progenitor that expresses renin throughout development and possesses a B-lymphocyte pedigree. This cell requires RBP-J to differentiate. PMID: 24549417
    14. functions as a transcriptional repressor on the promoter of the microRNA miR-155 PMID: 24996169
    15. DNA methylation-dependent binding of RBPJ to a GC repressor element can negatively regulate smooth muscl myosin heavy chain promoter activity and can inhibit marker gene expression in phenotypically modulated cells PMID: 25324571
    16. Rbpj directly regulates the expression of uterine matrix metalloproteinase in a Notch pathway-dependent manner, which is required for normal post-implantation decidual remodeling. PMID: 24971735
    17. RBP-J maintains the identity of the renin cell by not only activating genes characteristic of the myo-endocrine phenotype but also, preventing ectopic gene expression and adoption of an aberrant phenotype PMID: 24904090
    18. RBP-J-mediated Notch signaling is required for macrophages to promote hepatic fibrosis by up-regulation of NF-kappaB activation through CYLD. PMID: 25145286
    19. Environmental cues that regulate RBP-J expression/function potentially modulate the requirement for costimulatory signaling for osteoclast differentiation and bone remodeling. PMID: 25329696
    20. RBPJ in mouse Sertoli cells is required for proper regulation of the testis stem cell niche. PMID: 25406395
    21. Rbpj is required in postnatal endothelial cells to maintain proper artery, capillary and vein organization and to prevent abnormal arteriovenous shunting and malformation pathogenesis. PMID: 25209249
    22. we found that a fraction of RBPJ occupancy sites shifted between interphase and mitosis, suggesting that RBPJ can be retained on mitotic chromatin by sliding on DNA rather than disengaging from chromatin during mitotic chromatin condensation PMID: 24603501
    23. The CSL-KyoT2 corepressor complex is a negative regulator of Notch signaling. PMID: 24290140
    24. Disruption of the transcription factor RBP-J results in osteopenia attributable to attenuated osteoclast differentiation. PMID: 23224519
    25. RBP-J is essential for proper formation and maintenance of the kidney vasculature and glomeruli PMID: 24226518
    26. RBP-Jkappa-dependent Notch signaling is required for murine articular cartilage and joint maintenance. PMID: 23839930
    27. Data indicate the function of Rbpj is diversified and context dependent in the gliogenesis of somatosensory ganglia. PMID: 23826407
    28. Notch/Rbpjkappa signaling regulates progenitor maintenance and differentiation of hypothalamic arcuate neurons, which contribute to homeostatic regulation of body size. PMID: 23884446
    29. Notch negatively regulates chondrocyte differentiation in the axial skeleton by suppressing Sox9 transcription, and Rbpj-independent Notch signaling mechanisms may also contribute to axial skeletogenesis PMID: 22991339
    30. demonstrate dynamic binding of RBPJ in response to Notch activation at essentially all sites co-occupied by NICD PMID: 23651858
    31. RBP-J deficient dendritic cells exhibit attenuated cytoskeleton reorganization when contacting T cells. PMID: 23138187
    32. Data found that loss of RBPj in mature excitatory neurons was well tolerated, with no evidence for neurodegeneration or of learning and memory impairment in mice aged up to 18 months. PMID: 23110206
    33. Based on the transgenic mouse model, our data indicate that MZ B cells with certain BCR specificity can develop in a Notch-RBP-J independent manner PMID: 22719978
    34. 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. PMID: 22610140
    35. 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. PMID: 22682244
    36. RBP-J-mediated Notch signaling in aortic valves may be critically involved in valve homeostasis and valve diseases as well. PMID: 21773950
    37. Mice harboring intestinal epithelial cell-specific deletion of Rbpj, a transcription factor that mediates signaling through Notch receptors, develop chronic colitis characterized by the accumulation of T helper (Th)17 cells in colonic lamina propria. PMID: 22279105
    38. data demonstrate that Notch regulation of chondrocyte maturation is solely mediated via the RBPj-kappa-dependent pathway, and the perichodrium or osteogenic lineage probably influences chondrocyte terminal maturation and turnover of the cartilage matrix PMID: 22354840
    39. RBP-J strongly suppresses tumor necrosis factor-induced osteoclastogenesis and inflammatory bone resorption, but has minimal effects on physiological bone remodeling. PMID: 22249448
    40. When HNF-6 loss is combined with RBP-J loss, a phenotype consisting of cholestasis, hepatic necrosis, and fibrosis is observed that is more severe than the phenotype seen with Notch signaling loss alone. PMID: 21898486
    41. The data of this study indicated that Rbpj-mediated canonical Notch signaling inhibits DRG neuronal differentiation. PMID: 21510873
    42. differentiating hair cells and supporting cells rapidly die in RBPjkappa mutants, suggesting a requirement of RBPjk for cell survival in this tissue. PMID: 21632926
    43. Notch signaling disruption via RBPJk heterozygous inactivation results in aortic valve disease. PMID: 21493891
    44. Study shows a novel RBP-J function that promotes INP differentiation. PMID: 21443869
    45. MINT forms a high affinity complex with CSL; the domains of MINT and CSL that are necessary and sufficient for complex formation are delineated PMID: 21372128
    46. roles for Rbpj and notch signaling in multiple aspects of inner ear development including prosensory cell maturation, cellular differentiation and survival PMID: 21420948
    47. RBP-J-mediated canonical Notch signaling governs retinal cell specification and differentiation, and maintains retinal lamination through the expression of beta-catenin. PMID: 20017954
    48. reduction in graft survival was associated with augmented alloantigen specific T-cell proliferation and increased number of Th1, Th2, and Th17 cells in the RBP-J deficient recipient mice PMID: 21168915
    49. This study suggested RBP-J is not required for granule neuron progenitor development and medulloblastoma initiated by Hedgehog pathway activation in the external germinal layer PMID: 20950430
    50. Repression of p53 by RBP-Jkappa and activation of p53 by C/EBPbeta through differential binding of these two factors indicates a type of co-operative regulation in p53 expression. PMID: 20446924

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  • 亚细胞定位:
    Nucleus. Cytoplasm.
  • 蛋白家族:
    Su(H) family
  • 数据库链接:

    KEGG: mmu:19664

    STRING: 10090.ENSMUSP00000040694

    UniGene: Mm.209292