产品: NF kappaB p100/p52 抗体
货号: AF6373
描述: Rabbit polyclonal antibody to NF kappaB p100/p52
应用: WB IHC IF/ICC IP
文献验证: WB, IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken
蛋白号: Q00653
RRID: AB_2835217

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IP, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
NF kappaB p100/p52 Antibody detects endogenous levels of total NF kappaB p100/p52.
RRID:
AB_2835217
引用格式: Affinity Biosciences Cat# AF6373, RRID:AB_2835217.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

CVID10; DNA binding factor KBF2; H2TF1; Lymphocyte translocation chromosome 10 protein; LYT 10; NF kB2; NFKB p52/p100 subunit; Nuclear factor Kappa B subunit 2; Nuclear factor of kappa light polypeptide gene enhancer in B cells 2 (p49/p100); Nuclear factor of kappa light polypeptide gene enhancer in B cells 2; Oncogene Lyt 10; p100; Transcription factor NFKB2;

抗原和靶标

免疫原:

A synthesized peptide derived from human NF kappaB p100/p52, corresponding to a region within C-terminal amino acids.

基因/基因ID:
描述:
NFkB-p100 a transcription factor of the nuclear factor-kappaB ( NFkB) group. Precursor of the p52 subunit of the nuclear factor NF-kappa-B, which 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.

研究领域

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Human Diseases > Cancers: Specific types > Breast cancer.   (View pathway)

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

文献引用

1). Alpha-(1,6)-fucosyltransferase (FUT8) affects the survival strategy of osteosarcoma by remodeling TNF/NF-κB2 signaling. Cell death & disease, 2021 (PubMed: 34857735) [IF=8.1]

Application: WB    Species: Mouse    Sample:

Fig. 6: Knockdown of FUT8 in OS cells in vitro activates TNF/NF-κB2 signaling pathway. A Western blot of proteins in a NF-κB2 signaling pathway show that this pathway was activated in MNNG-siF8 cells but inhibited in MNNG-F8 cells. B Analysis of p52 translocation in OS cell lines. Western blot probed for both in nuclear p52 and cytoplasmic p52. C Quantitation of ratio of nuclear p52 to cytoplasmic p52 expression. Mean ± SD (N = 3) ratio expression in MNNG-siF8 cells was higher, compared to controls, and lower in MNNG-F8 cells. Relative expression of nuclear p52 was normalized to PCNA while relative expression of cytoplasmic p52 was normalized to β-tubulin. D Representative p52 immunofluorescent images of cultured OS cell lines showed translocation of p52 into the nucleus. Red fluorescence represented nuclei, green fluorescence represented p52 (Scale bar: 25 μm). The translocation of p52 into the nuclei appeared visually to be enhanced in MNNG-siF8 cells but reduced in MNNG-F8 cells compared to control cells. E Quantitation of ratio of nuclear p52 to cytoplasmic p52 in cultured OS cell lines. Mean ± SD (N = 3) ratio of nuclear p52 fluorescence to cytoplasmic p52 fluorescence. *P 

Application: IF/ICC    Species: Mouse    Sample:

Fig. 6: Knockdown of FUT8 in OS cells in vitro activates TNF/NF-κB2 signaling pathway. A Western blot of proteins in a NF-κB2 signaling pathway show that this pathway was activated in MNNG-siF8 cells but inhibited in MNNG-F8 cells. B Analysis of p52 translocation in OS cell lines. Western blot probed for both in nuclear p52 and cytoplasmic p52. C Quantitation of ratio of nuclear p52 to cytoplasmic p52 expression. Mean ± SD (N = 3) ratio expression in MNNG-siF8 cells was higher, compared to controls, and lower in MNNG-F8 cells. Relative expression of nuclear p52 was normalized to PCNA while relative expression of cytoplasmic p52 was normalized to β-tubulin. D Representative p52 immunofluorescent images of cultured OS cell lines showed translocation of p52 into the nucleus. Red fluorescence represented nuclei, green fluorescence represented p52 (Scale bar: 25 μm). The translocation of p52 into the nuclei appeared visually to be enhanced in MNNG-siF8 cells but reduced in MNNG-F8 cells compared to control cells. E Quantitation of ratio of nuclear p52 to cytoplasmic p52 in cultured OS cell lines. Mean ± SD (N = 3) ratio of nuclear p52 fluorescence to cytoplasmic p52 fluorescence. *P 

2). Fingolimod protects against cerebral ischemia reperfusion injury in rats by reducing inflammatory cytokines and inhibiting the activation of p38 MAPK and NF-κB signaling pathways. NEUROSCIENCE LETTERS, 2022 (PubMed: 34942319) [IF=2.5]

3). Astragaloside IV regulates NF‑κB‑mediated cellular senescence and apoptosis of hepatic stellate cells to suppress PDGF‑BB‑induced activation. Experimental and Therapeutic Medicine, 2019 (PubMed: 31641375) [IF=2.4]

Application: WB    Species: rat    Sample: HSC‑T6

Figure 6. |The expression of components in the NF‑κB pathway in platelet‑derived growth factor‑BB‑activated HSC‑T6 treated with ASIV. (A‑E) The relative mRNA expression levels of (A) p65, (B) p52, (C) p50, (D) IKKα and (E) IκBα. (F) Protein expression of p65, p52 and IκBα. *P<0.05 and **P<0.01. IKKα, inhibitor of nuclear factor‑κB kinase subunit‑α; IκBα, inhibitor of nuclear factor‑κB‑α; NF‑κB, nuclear factor‑κB; ASIV, astragaloside IV.

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