产品: NF-kB p65 抗体
货号: AF0874
描述: Rabbit polyclonal antibody to NF-kB p65
应用: WB IHC IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Horse, Sheep, Dog
分子量: 65kDa; 60kD(Calculated).
蛋白号: Q04206
RRID: AB_2834415

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, 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
预测:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Dog(100%)
克隆:
Polyclonal
特异性:
NF-kB p65 Antibody detects endogenous levels of total NF-kB p65.
RRID:
AB_2834415
引用格式: Affinity Biosciences Cat# AF0874, RRID:AB_2834415.
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

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:
Uniprot:
基因/基因ID:
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. Phosphorylation of serine residues on the I-kappa-B proteins by kinases (IKBKA, MIM 600664, or IKBKB, MIM 603258) marks them for destruction via the ubiquitination pathway, thereby allowing activation of the NFKB complex. Activated NFKB complex translocates into the nucleus and binds DNA at kappa-B-binding motifs such as 5-prime GGGRNNYYCC 3-prime or 5-prime HGGARNYYCC 3-prime (where H is A, C, or T; R is an A or G purine; and Y is a C or T pyrimidine).
序列:
MDELFPLIFPAEPAQASGPYVEIIEQPKQRGMRFRYKCEGRSAGSIPGERSTDTTKTHPTIKINGYTGPGTVRISLVTKDPPHRPHPHELVGKDCRDGFYEAELCPDRCIHSFQNLGIQCVKKRDLEQAISQRIQTNNNPFQVPIEEQRGDYDLNAVRLCFQVTVRDPSGRPLRLPPVLSHPIFDNRAPNTAELKICRVNRNSGSCLGGDEIFLLCDKVQKEDIEVYFTGPGWEARGSFSQADVHRQVAIVFRTPPYADPSLQAPVRVSMQLRRPSDRELSEPMEFQYLPDTDDRHRIEEKRKRTYETFKSIMKKSPFSGPTDPRPPPRRIAVPSRSSASVPKPAPQPYPFTSSLSTINYDEFPTMVFPSGQISQASALAPAPPQVLPQAPAPAPAPAMVSALAQAPAPVPVLAPGPPQAVAPPAPKPTQAGEGTLSEALLQLQFDDEDLGALLGNSTDPAVFTDLASVDNSEFQQLLNQGIPVAPHTTEPMLMEYPEAITRLVTGAQRPPDPAPAPLGAPGLPNGLLSGDEDFSSIADMDFSALLSQISS

种属预测

种属预测:

score>80的预测可信度较高,可尝试用于WB检测。*预测模型主要基于免疫原序列比对,结果仅作参考,不作为质保凭据。

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Xenopus
0
Zebrafish
0
Chicken
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - Q04206 作为底物

Site PTM Type Enzyme
M1 Acetylation
K37 Methylation
K37 Sumoylation
C38 S-Nitrosylation
S42 Phosphorylation
S45 Phosphorylation
K56 Ubiquitination
K62 Ubiquitination
T71 Phosphorylation
S75 Phosphorylation
K79 Ubiquitination
K93 Ubiquitination
S112 Phosphorylation
K122 Acetylation
K122 Ubiquitination
K123 Acetylation
K123 Ubiquitination
S131 Phosphorylation
T136 Phosphorylation
R174 Methylation
S180 Phosphorylation
R187 Methylation
K195 Ubiquitination
S205 Phosphorylation
K218 Acetylation
K218 Methylation
K218 Ubiquitination
K221 Acetylation
K221 Methylation
S238 Phosphorylation
S240 Phosphorylation
T254 Phosphorylation
S261 Phosphorylation
S269 Phosphorylation
S276 Phosphorylation P11309 (PIM1) , O94806 (PRKD3) , O75676 (RPS6KA4) , P17612 (PRKACA) , O75582 (RPS6KA5)
S281 Phosphorylation
T305 O-Glycosylation
T305 Phosphorylation
Y306 Phosphorylation
T308 Phosphorylation
K310 Acetylation
K310 Methylation
K310 Ubiquitination
S311 Phosphorylation Q05513 (PRKCZ)
K314 Acetylation
K314 Methylation
K314 Ubiquitination
K315 Acetylation
K315 Methylation
K315 Ubiquitination
S316 Phosphorylation P48729 (CSNK1A1)
S319 O-Glycosylation
T322 O-Glycosylation
S337 O-Glycosylation
S337 Phosphorylation
T352 O-Glycosylation
S374 O-Glycosylation
S374 Phosphorylation
S377 O-Glycosylation
T429 Phosphorylation
T435 Phosphorylation P28482 (MAPK1)
S468 Phosphorylation P49841 (GSK3B) , O14920 (IKBKB) , Q14164 (IKBKE)
S472 Phosphorylation
T505 Phosphorylation
S529 Phosphorylation P68400 (CSNK2A1) , P47710 (CSN1S1)
S536 Phosphorylation O15111 (CHUK) , O94806 (PRKD3) , Q9Y6K9 (IKBKG) , Q9UHD2 (TBK1) , Q9HCP0 (CSNK1G1) , Q16566 (CAMK4) , P51812 (RPS6KA3) , Q15418 (RPS6KA1) , Q00534 (CDK6) , O14920 (IKBKB) , P24723 (PRKCH) , Q14164 (IKBKE)
S543 Phosphorylation P68400 (CSNK2A1)
S547 Phosphorylation Q13315 (ATM)

研究背景

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 heterodimeric RELA-NFKB1 complex appears to be most abundant one. 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. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators. 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. The inhibitory effect of I-kappa-B on NF-kappa-B through retention in the cytoplasm is exerted primarily through the interaction with RELA. RELA shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Beside its activity as a direct transcriptional activator, it is also able to modulate promoters accessibility to transcription factors and thereby indirectly regulate gene expression. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cells. The NF-kappa-B homodimeric RELA-RELA complex appears to be involved in invasin-mediated activation of IL-8 expression.

翻译修饰:

Ubiquitinated by RNF182, leading to its proteasomal degradation. Degradation is required for termination of NF-kappa-B response.

Monomethylated at Lys-310 by SETD6. Monomethylation at Lys-310 is recognized by the ANK repeats of EHMT1 and promotes the formation of repressed chromatin at target genes, leading to down-regulation of NF-kappa-B transcription factor activity. Phosphorylation at Ser-311 disrupts the interaction with EHMT1 without preventing monomethylation at Lys-310 and relieves the repression of target genes (By similarity).

Phosphorylation at Ser-311 disrupts the interaction with EHMT1 and promotes transcription factor activity (By similarity). Phosphorylation on Ser-536 stimulates acetylation on Lys-310 and interaction with CBP; the phosphorylated and acetylated forms show enhanced transcriptional activity. Phosphorylation at Ser-276 by RPS6KA4 and RPS6KA5 promotes its transactivation and transcriptional activities.

Reversibly acetylated; the acetylation seems to be mediated by CBP, the deacetylation by HDAC3 and SIRT2. Acetylation at Lys-122 enhances DNA binding and impairs association with NFKBIA. Acetylation at Lys-310 is required for full transcriptional activity in the absence of effects on DNA binding and NFKBIA association. Acetylation at Lys-310 promotes interaction with BRD4. Acetylation can also lower DNA-binding and results in nuclear export. Interaction with BRMS1 promotes deacetylation of Lys-310. Lys-310 is deacetylated by SIRT2.

S-nitrosylation of Cys-38 inactivates the enzyme activity.

Sulfhydration at Cys-38 mediates the anti-apoptotic activity by promoting the interaction with RPS3 and activating the transcription factor activity.

Sumoylation by PIAS3 negatively regulates DNA-bound activated NF-kappa-B.

Proteolytically cleaved within a conserved N-terminus region required for base-specific contact with DNA in a CPEN1-mediated manner, and hence inhibits NF-kappa-B transcriptional activity.

细胞定位:

Nucleus. Cytoplasm.
Note: Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B) (PubMed:1493333). Colocalized with DDX1 in the nucleus upon TNF-alpha induction (PubMed:19058135). Colocalizes with GFI1 in the nucleus after LPS stimulation (PubMed:20547752). Translocation to the nucleus is impaired in L.monocytogenes infection (PubMed:20855622).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
亚基结构:

Component of the NF-kappa-B p65-p50 complex. Component of the NF-kappa-B p65-c-Rel complex. Homodimer; component of the NF-kappa-B p65-p65 complex. Component of the NF-kappa-B p65-p52 complex. May interact with ETHE1. Binds TLE5 and TLE1. Interacts with TP53BP2. Binds to and is phosphorylated by the activated form of either RPS6KA4 or RPS6KA5. Interacts with ING4 and this interaction may be indirect. Interacts with CARM1, USP48 and UNC5CL. Interacts with IRAK1BP1 (By similarity). Interacts with NFKBID (By similarity). Interacts with NFKBIA. Interacts with GSK3B. Interacts with NFKBIB (By similarity). Interacts with NFKBIE. Interacts with NFKBIZ. Interacts with EHMT1 (via ANK repeats) (By similarity). Part of a 70-90 kDa complex at least consisting of CHUK, IKBKB, NFKBIA, RELA, ELP1 and MAP3K14. Interacts with HDAC3; HDAC3 mediates the deacetylation of RELA. Interacts with HDAC1; the interaction requires non-phosphorylated RELA. Interacts with CBP; the interaction requires phosphorylated RELA. Interacts (phosphorylated at 'Thr-254') with PIN1; the interaction inhibits p65 binding to NFKBIA. Interacts with SOCS1. Interacts with UXT. Interacts with MTDH and PHF11. Interacts with ARRB2. Interacts with NFKBIA (when phosphorylated), the interaction is direct; phosphorylated NFKBIA is part of a SCF(BTRC)-like complex lacking CUL1. Interacts with RNF25. Interacts (via C-terminus) with DDX1. Interacts with UFL1 and COMMD1. Interacts with BRMS1; this promotes deacetylation of 'Lys-310'. Interacts with NOTCH2 (By similarity). Directly interacts with MEN1; this interaction represses NFKB-mediated transactivation. Interacts with AKIP1, which promotes the phosphorylation and nuclear retention of RELA. Interacts (via the RHD) with GFI1; the interaction, after bacterial lipopolysaccharide (LPS) stimulation, inhibits the transcriptional activity by interfering with the DNA-binding activity to target gene promoter DNA. Interacts (when acetylated at Lys-310) with BRD4; leading to activation of the NF-kappa-B pathway. Interacts with MEFV. Interacts with CLOCK (By similarity). Interacts (via N-terminus) with CPEN1; this interaction induces proteolytic cleavage of p65/RELA subunit and inhibition of NF-kappa-B transcriptional activity. Interacts with FOXP3. Interacts with CDK5RAP3; stimulates the interaction of RELA with HDAC1, HDAC2 and HDAC3 thereby inhibiting NF-kappa-B transcriptional activity. Interacts with DHX9; this interaction is direct and activates NF-kappa-B-mediated transcription. Interacts with LRRC25. Interacts with TBX21 (By similarity). Interacts with KAT2A (By similarity). Interacts with ZBTB7A; involved in the control by RELA of the accessibility of target gene promoters. Directly interacts with DDX3X; this interaction may trap RELA in the cytoplasm, impairing nuclear relocalization upon TNF activating signals.

(Microbial infection) Interacts with human respiratory syncytial virus (HRSV) protein M2-1.

(Microbial infection) Interacts with molluscum contagiosum virus MC132.

(Microbial infection) Interacts with herpes virus 8 virus protein LANA1.

蛋白家族:

The transcriptional activation domain 3/TA3 does not participate to the direct transcriptional activity of RELA but is involved in the control by RELA of the accessibility of target gene promoters. Mediates interaction with ZBTB7A.

The transcriptional activation domain 1/TA1 and the transcriptional activation domain 2/TA2 have direct transcriptional activation properties (By similarity). The 9aaTAD motif found within the transcriptional activation domain 2 is a conserved motif present in a large number of transcription factors that is required for their transcriptional transactivation activity (PubMed:17467953).

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). Hou B et al. Reproductive toxicity of polystyrene microplastics: In vivo experimental study on testicular toxicity in mice. JOURNAL OF HAZARDOUS MATERIALS 2020 Oct 5;124028. (PubMed: 33087287) [IF=13.6]

Application: WB    Species: mice    Sample: testis tissue

Fig. 6. NF-κBp65 related protein expression in the testis tissue mice by western blotting. *P < 0.05, compared with the corresponding control. #P < 0.05compared with the L-Dose group, $ P < 0.05 compared with the M-Dose group.

2). Wu H et al. Breaking the vicious loop between inflammation, oxidative stress and coagulation, a novel anti-thrombus insight of nattokinase by inhibiting LPS-induced inflammation and oxidative stress. Redox Biology 2020 Mar 11;32:101500 (PubMed: 32193146) [IF=11.4]

Application: IF/ICC    Species: Mice    Sample: RAW264.7 cells

Fig. 3. NK inhibited LPS-induced NF-κB activation in RAW264.7 cells. (A) Effect of NK on LPS-induced IκBα activation in RAW264.7 cells. Cells were pretreated with NK (0.08, 0.15, and 0.30 FU/mL) for 1 h before being exposed to LPS (0.1 μg/ml) for 6 h. Equal amounts of total cell lysates were loaded and subjected to immunoblot analysis. β-actin was used as the control for equal protein loading and protein integrity. **P < 0.01, vs. Control; #P < 0.05, ##P < 0.01, vs. LPSstimulated cells. (B) Effect of NK on LPS-induced P65 nuclear-translation in RAW264.7 cells. Cells were pretreated with NK (0.30 FU/mL) for 1 h and then exposed to LPS (0.1 μg/mL) for 6 h. Immunofluorescence analysis was performed. P65 protein was marked with green fluorescent, and the nucleus were dyed blue with Hochest. Scale bar: 40 μm. (C) Effect of NK on LPS-induced TNF-α release in RAW264.7 cells. Cells were pretreated with NK (0.08, 0.15, 0.30 FU/mL) for 1 h before LPS (0.1 μg/mL) stimulation for 24 h. Cell supernatant was collected to detect TNF-α level by ELISA. (D) Effect of NK on LPS-induced IL-6 release in RAW264.7 cells. Cells were pretreated with NK (0.08, 0.15, 0.30 FU/mL) for 1 h before LPS (0.1 μg/mL) stimulation for 24 h. Cell supernatant was collected to detect IL-6 level by ELISA. **p < 0.01, ***p < 0.001, vs. control; #p < 0.05, ##p < 0.01, ###p < 0.001, vs. LPS-stimulated cells. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

3). Ouyang et al. The YTHDF1–TRAF6 pathway regulates the neuroinflammatory response and contributes to morphine tolerance and hyperalgesia in the periaqueductal gray. Journal of Neuroinflammation 2022 Dec 22;19(1):310. (PubMed: 36550542) [IF=9.3]

4). Yang YF et al. Ficolin-A/2, acting as a new regulator of macrophage polarization, mediates the inflammatory response in experimental mouse colitis. IMMUNOLOGY 2017 Aug;151(4):433-450 (PubMed: 28380665) [IF=6.4]

5). Huang X et al. SU5416 attenuated lipopolysaccharide-induced acute lung injury in mice by modulating properties of vascular endothelial cells. Drug Design Development and Therapy 2019 May 23;13:1763-1772 (PubMed: 31213766) [IF=4.8]

Application: WB    Species: mouse    Sample: lung

Figure 3 |TLR4/NF-κB signaling was involved in the progression of LPS-stimulated ALI. (A) Immunohistochemical staining of CD31 in LPS-stimulated WT and TLR4−/- mice after treatment with DXM and/or SU5416+DXM.. (B) Mice were treated with DXM and/or SU5416 for 12 hours, and the expressions of TLR4, p-p65, NF-κB, p-VEGFR2,VEGF2R, p53, Bcl-2, and β-actin in lung tissues were detected with Western blot

6). Wang XS et al. Anxiolytic effects of Formononetin in an inflammatory pain mouse model. Molecular Brain 2019 Apr 8;12(1):36 (PubMed: 30961625) [IF=3.6]

7). Xie et al. Genistein alleviates chronic vascular inflammatory response via the miR‑21/NF‑κB p65 axis in lipopolysaccharide‑treated mice. Molecular Medicine Reports 2021 Mar;23(3):192. (PubMed: 33495831) [IF=3.4]

Application: WB    Species: Mice    Sample: HUVE-12 cells

Figure 2. Effects of GEN on chronic inflammation in the aortae of LPS-treated C57BL/6 mice. (A) Reverse transcription-quantitative PCR analysis of TNF-α and IL-6 mRNA expression. (B) Western blot analysis of the protein levels of iNOS and NF-κB p65. (C) Immunohistochemistry and (D) immunofluorescence staining for NF-κB p65 (magnification, ×400). Data are presented as the mean ± SD (n=10/group). *P<0.05, ***P<0.001. Ctrl, control; GEN, genistein; iNOS, inducible nitric oxide synthase; LPS, lipopolysaccharide.

Application: IF/ICC    Species: Mice    Sample: HUVE-12 cells

Figure 2. Effects of GEN on chronic inflammation in the aortae of LPS-treated C57BL/6 mice. (A) Reverse transcription-quantitative PCR analysis of TNF-α and IL-6 mRNA expression. (B) Western blot analysis of the protein levels of iNOS and NF-κB p65. (C) Immunohistochemistry and (D) immunofluorescence staining for NF-κB p65 (magnification, ×400). Data are presented as the mean ± SD (n=10/group). *P<0.05, ***P<0.001. Ctrl, control; GEN, genistein; iNOS, inducible nitric oxide synthase; LPS, lipopolysaccharide.

Application: IHC    Species: Mice    Sample: HUVE-12 cells

Figure 2. Effects of GEN on chronic inflammation in the aortae of LPS-treated C57BL/6 mice. (A) Reverse transcription-quantitative PCR analysis of TNF-α and IL-6 mRNA expression. (B) Western blot analysis of the protein levels of iNOS and NF-κB p65. (C) Immunohistochemistry and (D) immunofluorescence staining for NF-κB p65 (magnification, ×400). Data are presented as the mean ± SD (n=10/group). *P<0.05, ***P<0.001. Ctrl, control; GEN, genistein; iNOS, inducible nitric oxide synthase; LPS, lipopolysaccharide.

8). Guan SY et al. Anxiolytic effects of polydatin through the blockade of neuroinflammation in a chronic pain mouse model. Molecular Pain 2020 Jan-Dec;16:1744806919900717 (PubMed: 31964240) [IF=3.3]

Application: WB    Species: Mice    Sample: amygdala

Figure 5. Polydatin suppressed CFA-induced production of proinflammatory mediators and NF-κB signaling pathway in the amygdala. (a and b) Effects of polydatin against CFA-induced proinflammation by ELISA. Polydatin treatment reduced TNF-ɑ and IL-1β levels in the amygdala of CFA-injected mice. (c) Representative bands of Western blot analysis showing the levels of NF-κB p65 and p-IκBɑ. CFA injection evidently increased NF-κB p65and p-IκBɑ (d) in the amygdala, which were reversed by polydatin administration. Data are presented as means ± SEM (n = 7 in each group). **p < 0.01 vs. control group; #p<0.05, ##p < 0.01 vs. CFA group. CFA: complete Freund’s adjuvant; TNF-ɑ: tumor necrosis factor-alpha; IL-1β: interleukin-1β.

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