NFKB2 (Ab-870) Antibody

說(shuō)明書

中文名稱：

NFKB2 (Ab-870)兔多克隆抗體
貨號(hào)：

CSB-PA178291
規(guī)格：

￥2024
圖片：
Western blot analysis of extracts from HL60 cells using NFkB-p100(Ab-870) Antibody.

Immunohistochemical analysis of paraffin-embedded human breast carcinoma tissue using NFkB-p100(Ab-870) Antibody(left) or the same antibody preincubated with blocking peptide(right).
其他：

產(chǎn)品詳情
產(chǎn)品評(píng)價(jià)
相關(guān)產(chǎn)品
靶點(diǎn)詳情

產(chǎn)品詳情

產(chǎn)品名稱：

Rabbit anti-Homo sapiens (Human) NFKB2 Polyclonal antibody
Uniprot No.：

Q00653
基因名：

NFKB2
宿主：

Rabbit
反應(yīng)種屬：

Human,Mouse,Rat
免疫原：

Peptide sequence around aa.868~872 (Y-G-S-Q-S) derived from Human NFkB-p100.
免疫原種屬：

Homo sapiens (Human)
克隆類型：

Polyclonal
純化方式：

Antibodies were produced by immunizing rabbits with synthetic peptide and KLH conjugates. Antibodies were purified by affinity-chromatography using epitope-specific peptide.
濃度：

It differs from different batches. Please contact us to confirm it.
產(chǎn)品提供形式：

Liquid
應(yīng)用范圍：

ELISA,WB,IHC

推薦稀釋比：

Application	Recommended Dilution
WB	1:500-1:1000
IHC	1:50-1:200

Protocols：

ELISA Protocol
Western Blotting (WB) Protocol
Immunohistochemistry (IHC) Protocol
儲(chǔ)存條件：

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
貨期：

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
用途：

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產(chǎn)品評(píng)價(jià)

靶點(diǎn)詳情

功能：

NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes 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. In concert with RELB, regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-ARNTL/BMAL1 heterodimer.
基因功能參考文獻(xiàn)：
1. Functional evaluation of natural killer cell cytotoxic activity in NFKB2-mutated patients. PMID: 29278687
2. the present study demonstrated that NFKB2 may be involved in the development of HL by interacting with several genes and miRNAs, including BCL2L1, CSF2, miR-135a-5p, miR-155-5p and miR-9-5p. PMID: 29693141
3. TNF-alpha-induced expression of transport protein genes in HUVEC cells is associated with enhanced expression of RELB and NFKB2. PMID: 29658079
4. This study demonstrated that NF-kappaB mRNA levels were significantly decreased in the new cases of untreated MS patients in comparison to healthy controls. PMID: 28433998
5. our studies for the first time establish p100 as a key tumor suppressor of bladder cancer growth PMID: 27095572
6. 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. PMID: 27678221
7. report a detailed state-of-the-art mass spectrometry-based protein-protein interaction network including the noncanonical NF-kappaB signaling nodes TRAF2, TRAF3, IKKalpha, NIK, and NF-kappaB2/p100. PMID: 27416764
8. novel NFKB2 gain-of-function mutations produce a nonfully penetrant combined immunodeficiency phenotype through a different pathophysiologic mechanism than previously described for mutations in NFKB2 PMID: 28778864
9. a new ERK2/AP-1/miR-494/PTEN pathway that is responsible for the tumor-suppressive role of NFkappaB2 p100 in cellular transformation. PMID: 26686085
10. MKK4 activates non-canonical NFkappaB signaling by promoting NFkappaB2-p100 processing. PMID: 28733031
11. 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. PMID: 27292187
12. 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 PMID: 28507099
13. Thyroidal NF-kappaB2 (noncanonical) activity is more pronounced in Graves disease than in normal thyroids. PMID: 27929668
14. Gene expression levels of NF-kappaB2 were deregulated in 49 B-cell chronic lymphocytic leukemia, 8 B-cell non-Hodgkin's lymphoma, 3 acute myeloid leukemia, 3 chronic myeloid leukemia, 2 hairy cell leukemia, 2 myelodysplastic syndrome, and 2 T-cell large granular lymphocytic leukemia patients in the post-Chernobyl period. PMID: 25912249
15. melatonin transcriptionally inhibited MMP-9 by reducing p65- and p52-DNA-binding activities. Moreover, the Akt-mediated JNK1/2 and ERK1/2 signaling pathways were involved in melatonin-regulated MMP-9 transactivation and cell motility. PMID: 26732239
16. 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. PMID: 26307012
17. HDAC4-RelB-p52 complex maintains repressive chromatin around proapoptotic genes Bim and BMF and regulates multiple myeloma survival and growth PMID: 26455434
18. The augmentation of methylation in the NFkB2 promoter by interval walking training is advantageous in promoting a healthy state by ameliorating the susceptibility to inflammation PMID: 25901949
19. Data show that NF-kappa-B p52 subunit (p52) interacts with ets transcription factors ETS1/2 factors at the C250T telomerase (TERT) promoter to mediate TERT reactivation. PMID: 26389665
20. mutation results in common variable immunodeficiency with reduction in B cells, memory B cells and T follicular helper cells PMID: 24888602
21. Results confirm previous findings that de novo mutations near the C-terminus of NFKB2 cause combined endocrine and immunodeficiencies. PMID: 25524009
22. 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. PMID: 25349408
23. NIK plays a key role in constitutive NF-kappaB activation and the progression of ovarian cancer cells PMID: 24533079
24. We report 3 related individuals with a novel form of severe B-cell deficiency associated with partial persistence of serum immunoglobulin arising from a missense mutation in NFKB2. PMID: 25237204
25. NFkappaB2/p100 was overexpressed and accumulated in a well-established in vitro human monocyte model of Endotoxin tolerance. The p100 accumulation in these cells inversely correlated with the inflammatory response after LPS stimulation. PMID: 25225662
26. NFKB2 genetic variation associated with sleep disorders in patients, diagnosed with breast cancer. PMID: 24012192
27. higher level of expression is associated with death in non-small cell lung cancer PMID: 24355259
28. NF-kappaB2/p100 deficiency caused a predominant B-cell-intrinsic TI-2 defect that could largely be attributed to impaired proliferation of plasmablasts. Importantly, p100 was also necessary for efficient defense against clinically relevant TI-2 pathogens. PMID: 24242887
29. NFKB2 binds to the PLK4 promoter at upstream and downstream of the PLK4 transcription initiation site abd reduced PLK4 mRNA and protein levels. PMID: 23974100
30. our study demonstrates a link between persistent activation of the AR by NF-kappaB2/p52 and development of resistance to enzalutamide in prostate cancer. PMID: 23699654
31. Single nucleotide polymorphisms of angiotensin-converting enzyme (ACE), nuclear factor kappa B (NFkB)and cholesteryl ester transport protein (CETP) were evaluated in nonagenarians, centenarians, and average life span individuals (controls). PMID: 23389097
32. Heterozygous mutations in NFKB2 cause a unique form of early-onset CVID that also presents with central adrenal insufficiency. PMID: 24140114
33. Constitutive processing of C-terminal truncation mutants of p100 is associated with their active nuclear translocation. Mutation of the nuclear localization signal (NLS) of p100 abolishes its processing. PMID: 12894228
34. Sp1 is required for IL-15 induction by both poly(I:C) and respiratory syncytial virus, a response that also requires NFkappaB2 and IKKepsilon. PMID: 23873932
35. TRAF2/NIK/NF-kappaB2 pathway regulates pancreatic ductal adenocarcinoma cell tumorigenicity PMID: 23301098
36. the FBXW7alpha-dependent degradation of p100 functions as a prosurvival mechanism through control of NF-kappaB activity. PMID: 23211527
37. These findings provide a mouse model for human multiple myeloma with aberrant NF-kappaB2 activation and suggest a molecular mechanism for NF-kappaB2 signaling in the pathogenesis of plasma cell tumors. PMID: 22642622
38. RelB/NF-kappaB2, is constitutively activated in the human placenta, which binds to a previously undescribed NF-kappaB enhancer of corticotropin-releasing hormone (CRH) gene promoter to regulate CRH expression. PMID: 22734038
39. The noncanonical NF-kappaB pathway is integral in controlling immunoregulatory phenotypes of both plasmacytoid and conventional dendritic cells. PMID: 22879398
40. Fbw7-mediated destruction of p100 is a regulatory component restricting the response to NF-kappaB2 pathway stimulation. PMID: 22864569
41. Flt3ITD promotes a noncanonical pathway via TAK1 and p52NF-kappaB to suppress DAPK1 in association with histone deacetylases, which explains DAPK1 repression in Flt3ITD(+) acute myeloid leukemia. PMID: 22096027
42. NF-kappaB2 exhibits the major inhibitory role in the transcription at the CD99 promoter PMID: 22083306
43. mutant p53 elevates expression of genes capable of enhancing cell proliferation, motility, and tumorigenicity by inducing acetylation of histones via recruitment of CBP and STAT2 on the promoters causing CBP-mediated histone acetylation PMID: 22198284
44. Total expression of nuclear factor kappa B-2 was not significantly changed in melphalan resistance in multiple myeloma, but more of the protein population was converted into the p52 isoform PMID: 21846842
45. The activation profile of diffuse large B-cell lymphomas/posttransplantation lymphoproliferative disorders was not associated with BAFF/BAFF-R expression, whereas nuclear p52 activation might be linked to Epstein-Barr virus. PMID: 21871426
46. Data show that IKBalpha, NFKB2, and TRAF3 gene polymorphisms play a role in the development of multiple myeloma and in the response to bortezomib therapy. PMID: 21228035
47. Data show that MEKK-1 plays an integral role in IL-1beta modulation of Caco-2 TJ barrier function by regulating the activation of the canonical NF-kappaB pathway and the MLCK gene. PMID: 21048223
48. Role of NFKB2 on the early myeloid differentiation of CD34+ hematopoietic stem/progenitor cells PMID: 20708837
49. NF-kappaB2/p52 may play a critical role in the progression of castration-resistant prostate cancer through activation of the androgen receptor PMID: 20388792
50. Data demonstrate in various tumor cell lines and primary T-cells that TNFR2, but not TNFR1, induces activation of the alternative NFkappaB pathway and p100 processing. PMID: 20038584
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相關(guān)疾病：

Immunodeficiency, common variable, 10 (CVID10)
亞細(xì)胞定位：

Nucleus. Cytoplasm. Note=Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B).
數(shù)據(jù)庫(kù)鏈接：

HGNC: 7795

OMIM: 164012

KEGG: hsa:4791

STRING: 9606.ENSP00000358983

UniGene: Hs.73090

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