Phospho-NF-kB p65 (Ser276) Antibody - #AF3387

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产品: 磷酸化 NF-kB p65 (Ser276) 抗体
货号: AF3387
描述: Rabbit polyclonal antibody to Phospho-NF-kB p65 (Ser276)
应用: WB IHC IF/ICC IP
文献验证: WB, IHC
反应: Human, Mouse, Rat
预测: Pig, Zebrafish, Bovine, Horse, Sheep, Dog, Xenopus
蛋白号: Q04206
RRID: AB_2834818

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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:
Phospho-NF-kB p65 (Ser276) Antibody detects endogenous levels of NF-kB p65 only when phosphorylated at Serine 276.
RRID:
AB_2834818
引用格式: Affinity Biosciences Cat# AF3387, RRID:AB_2834818.
偶联:
Unconjugated.
纯化:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
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

Avian reticuloendotheliosis viral (v rel) oncogene homolog A; MGC131774; NF kappa B p65delta3; NFKB3; Nuclear Factor NF Kappa B p65 Subunit; Nuclear factor NF-kappa-B p65 subunit; Nuclear factor of kappa light polypeptide gene enhancer in B cells 3; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3; OTTHUMP00000233473; OTTHUMP00000233474; OTTHUMP00000233475; OTTHUMP00000233476; OTTHUMP00000233900; p65; p65 NF kappaB; p65 NFkB; relA; TF65_HUMAN; Transcription factor p65; v rel avian reticuloendotheliosis viral oncogene homolog A (nuclear factor of kappa light polypeptide gene enhancer in B cells 3 (p65)); V rel avian reticuloendotheliosis viral oncogene homolog A; v rel reticuloendotheliosis viral oncogene homolog A (avian); V rel reticuloendotheliosis viral oncogene homolog A, nuclear factor of kappa light polypeptide gene enhancer in B cells 3, p65;

抗原和靶标

免疫原:

A synthesized peptide derived from human NF- kappaB p65 around the phosphorylation site of Ser276.

基因/基因ID:
RELA(5970)
描述:
NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA, or RELB (MIM 604758) to form the NFKB complex. The p50 (NFKB1)/p65 (RELA) heterodimer is the most abundant form of NFKB. The NFKB complex is inhibited by I-kappa-B proteins (NFKBIA, MIM 164008 or NFKBIB, MIM 604495), which inactivate NFKB by trapping it in the cytoplasm.

研究领域

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

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

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

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

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

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway.   (View pathway)

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

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

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

· Human Diseases > Drug resistance: Antineoplastic > Antifolate resistance.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Substance dependence > Cocaine addiction.

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Shigellosis.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

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

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

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

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

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

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

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

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Acute myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Small cell lung cancer.   (View pathway)

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway.   (View pathway)

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

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > RIG-I-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Cytosolic DNA-sensing pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > B cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Prolactin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

文献引用

1). Pin1 promotes pancreatic cancer progression and metastasis by activation of NF‐κB‐IL‐18 feedback loop. Cell Proliferation, 2020 (PubMed: 32347623) [IF=5.9]

Application: WB    Species: human    Sample: pancreatic cancer cell

FIGURE 4 Pin1 binds to p65 and facilitates NF-κB activation in pancreatic cancer cells. (A) Co-immunoprecipitation analysis of the interaction between Pin1 and p65 in pancreatic cancer cells. (B) Double immunofluorescent staining revealed co-localization of the Pin1 and p65 proteins in Capan-1 and SW19990 cells (scale bar, 5 μm). (C) The effects of Pin1 knockdown on phosphorylation of p65 were assessed by Western blot. (D) Nuclear translocation of p65 induced by Pin1. MIA PaCa-2 cells were transfected with Pin1 or empty vector, and p65 location was determined (scale bar, 25 μm). (E) Increase of NF-κB by Pin1 upregulation. Cells were cotransfected with Pin1 vector or control and NF-κB-Luc construct, followed by luciferase assay
2). Qinhuo Shanggan oral solution resolves acute lung injury by down-regulating TLR4/NF-κB signaling cascade and inhibiting NLRP3 inflammasome activation. Frontiers in Immunology, 2023 (PubMed: 37954597) [IF=5.7]

Application: IHC    Species: Rat    Sample:

Figure 5 QHSG down-regulates TLR4/NF-κB signaling cascade in LPS-induced acute lung injury of the rats. (A) The qRT-PCR analysis of TLR4 mRNA level in the lung tissues of the rats with LPS-induced ALI, treated by QHSG at 5.5 g/kg, 11 g/kg and 22 g/kg or dexamethasone at 2 mg/kg. N=4. (B) Western blotting of the protein expressions of TLR4, IκBα, p65 and phospho-p65 in the lung tissues of the rats with LPS-induced ALI, treated by QHSG at 5.5 g/kg, 11 g/kg and 22 g/kg or dexamethasone at 2 mg/kg. N=3. (C) Western blotting of nuclear p65 protein level in the lung tissues of the rats with LPS-induced ALI, treated by QHSG at 5.5 g/kg, 11 g/kg and 22 g/kg or dexamethasone at 2 mg/kg. N=3. (D) IHC analyses of protein levels of TLR4 and phospho-p65 in the lung tissues of the rats with LPS-induced ALI, treated by QHSG at 5.5 g/kg, 11 g/kg and 22 g/kg or dexamethasone at 2 mg/kg. Scale bars = 20 μm. N=3. C, the normal control; M, the model rats. ## p< 0.01 versus the normal control. *p < 0.05 and **p < 0.01 versus the model rats.

Application: WB    Species: Rat    Sample:

Figure 5 QHSG down-regulates TLR4/NF-κB signaling cascade in LPS-induced acute lung injury of the rats. (A) The qRT-PCR analysis of TLR4 mRNA level in the lung tissues of the rats with LPS-induced ALI, treated by QHSG at 5.5 g/kg, 11 g/kg and 22 g/kg or dexamethasone at 2 mg/kg. N=4. (B) Western blotting of the protein expressions of TLR4, IκBα, p65 and phospho-p65 in the lung tissues of the rats with LPS-induced ALI, treated by QHSG at 5.5 g/kg, 11 g/kg and 22 g/kg or dexamethasone at 2 mg/kg. N=3. (C) Western blotting of nuclear p65 protein level in the lung tissues of the rats with LPS-induced ALI, treated by QHSG at 5.5 g/kg, 11 g/kg and 22 g/kg or dexamethasone at 2 mg/kg. N=3. (D) IHC analyses of protein levels of TLR4 and phospho-p65 in the lung tissues of the rats with LPS-induced ALI, treated by QHSG at 5.5 g/kg, 11 g/kg and 22 g/kg or dexamethasone at 2 mg/kg. Scale bars = 20 μm. N=3. C, the normal control; M, the model rats. ## p< 0.01 versus the normal control. *p < 0.05 and **p < 0.01 versus the model rats.
3). Herpes Simplex Virus 1 UL2 Inhibits the TNF-α–Mediated NF-κB Activity by Interacting With p65/p50. Frontiers in Immunology, 2020 (PubMed: 32477319) [IF=5.7]

Application: WB    Species: Human    Sample: HEK293T cells

FIGURE 9 | p65 phosphorylation at Ser536 is suppressed by HSV-1 UL2. (A,C) HEK293T cells transfected with either HA empty vector or UL2-HA expression plasmid were stimulated with TNF-α (20 ng/mL) for the indicated times (0, 30, and 60 min) according to previous studies (59, 77), and then equal amounts of cell lysates were analyzed by WBs with phospho-NF-κB–p65 (Ser536) Ab (A), phospho-NF-κB–p65 (Ser276) Ab (C) (top panel), or anti-p65 pAb (second panel). Protein levels of UL2 (third panel) and β-actin (bottom panel) in the same cell lysates were also determined. (B,D) Densitometry of phospho-NF-κB–p65 Ser536 (B) and Ser276 bands (D) from (A,C), respectively, were normalized to loading control β-actin. Data were expressed as means ± SD from three independent experiments. ns, not significant and ***P < 0.001.

Application: WB    Species: human    Sample: HEK293T cells

FIGURE 9 | p65 phosphorylation at Ser536 is suppressed by HSV-1 UL2. (A,C) HEK293T cells transfected with either HA empty vector or UL2-HA expression plasmid were stimulated with TNF-α (20 ng/mL) for the indicated times (0, 30, and 60 min) according to previous studies (59, 77), and then equal amounts of cell lysates were analyzed by WBs with phospho-NF-κB–p65 (Ser536) Ab (A), phospho-NF-κB–p65 (Ser276) Ab (C) (top panel), or anti-p65 pAb (second panel). Protein levels of UL2 (third panel) and β-actin (bottom panel) in the same cell lysates were also determined. (B,D) Densitometry of phospho-NF-κB–p65 Ser536 (B) and Ser276 bands (D) from (A,C), respectively, were normalized to loading control β-actin.
4). Distinct roles of A1/A2 astrocytes in blood-brain barrier injury following cerebral I/R via the ROCK/NF-κB and STAT3 pathways. International immunopharmacology, 2025 (PubMed: 40020465) [IF=4.8]
5). PIM1 inhibitor SMI-4a attenuated lipopolysaccharide-induced acute lung injury through suppressing macrophage inflammatory responses via modulating p65 phosphorylation. International Immunopharmacology, 2019 (PubMed: 31203114) [IF=4.8]
6). Neuroprotective effects of Shenghui decoction via inhibition of the JNK/p38 MAPK signaling pathway in an AlCl3-induced zebrafish (Danio rerio) model of Alzheimer's disease. Journal of ethnopharmacology, 2024 (PubMed: 38423408) [IF=4.8]
7). 7-Difluoromethoxy-5, 4′-dimethoxy-genistein attenuates macrophages apoptosis to promote plaque stability via TIPE2/TLR4 axis in high fat diet-fed ApoE−/− mice. International Immunopharmacology, 2021 (PubMed: 33813367) [IF=4.8]

Application: WB    Species: mice    Sample: RAW264.7 cells

Fig. 9. DFMG regulated TLR4 signaling pathway to inhibit apoptosis by TIPE2 in LPC-induced RAW264.7 cells. Cells, overexpress or knockdown of TIPE2, were preincubated with DFMG for 0.5 h, then stimulated with LPC for 24 h. (A and D) RT-qPCR and Western blot were used to detect the level of TIPE2 mRNA and protein, respectively. RT-qPCR (B) and Western blot (C) were used to detect the expression of TLR4, MyD88, NF-κB p65, p-NF-κB p65Ser276, cleaved Caspase-3 in TIPE2-OE cells. RT-qPCR (E) and Western blot (F) were used to assay the expression of TLR4, MyD88, NF-κB p65, p-NF-κB p65Ser276, cleaved Caspase-3 in TIPE2-KD cells. n = 3, Data are presented as mean ± SD from three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001; TIPE2-NC: TIPE2-negative control, TIPE2-OE: TIPE2- overexpression, TIPE2-KD: TIPE2-knockdown.
8). Network pharmacology combines machine learning, molecular simulation dynamics and experimental validation to explore the mechanism of acetylbinankadsurin A in the treatment of liver fibrosis. Journal of ethnopharmacology, 2024 (PubMed: 38169205) [IF=4.8]
9). Extract of Nanhaia speciosa J. Compton & Schrire alleviates LPS-induced acute lung injury via the NF-κB/Nrf2/AQPs pathway. Journal of ethnopharmacology, 2024 (PubMed: 39278292) [IF=4.8]
10). PDE4B Modulates Phosphorylation of p65 (Ser468) via cAMP/PKA in Acute Lung Injury. Lung, 2025 (PubMed: 39956855) [IF=4.6]
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