| 别名 | NFKB1;Nuclear factor NF-kappa-B p105 subunit;DNA-binding factor KBF1;EBP-1;Nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 |
| 基因名称 | NFKB1 |
| 蛋白名称 | Nuclear factor NF-kappa-B p105 subunit |
| 推荐应用 | |
| 反应物种 | Mouse |
| 存储缓冲液 | PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA |
| Human Gene Link | 4790 |
| Human Swissprot No. | P25799 |
| Mouse Gene ID | 18033 |
| Mouse Swissprot No. | P25799 |
| Rat Swissprot No. | Q63369 |
| 特异性 | endogenous |
| 稀释度 | IHC 1:200-1:1000;WB 1:1000-1:5000;IF 1:200-1:1000;ELISA 1:5000-1:20000;IP 1:50-1:200; |
| 参考分子量 | MW(Observed):50kD,120kD |
| 预测分子量 | MW(Calculated):50kD,105kD |
| 运输及保存条件 | -15°C to -25°C/1 year(Do not lower than -25°C) |
| 宿主 | Rabbit |
| 同种型 | IgG,Kappa |
| 背景介绍 | nuclear factor kappa B subunit 1(NFKB1) Homo sapiens This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. Alternative splicing results in multiple transcript variants encoding different isof |
| 细胞定位 | Cytoplasm, Nucleus |
| 功能 | Domain:Glycine-rich region (GRR) appears to be a critical element in the generation of p50.,Domain:The C-terminus of p105 might be involved in cytoplasmic retention, inhibition of DNA-binding, and transcription activation.,Function:NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed 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 and the heterodimeric p65-p50 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. 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. NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. The NF-kappa-B p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 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. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105.,induction:By phorbol ester and TNF-alpha.,PTM:Phosphorylation at 'Ser-903' and 'Ser-907' primes p105 for proteolytic processing in response to TNF-alpha stimulation. Phosphorylation at 'Ser-927' and 'Ser-932' are required for BTRC/BTRCP-mediated proteolysis.,PTM:Polyubiquitination seems to allow p105 processing.,PTM:S-nitrosylation of Cys-61 affects DNA binding.,PTM:While translation occurs, the particular unfolded structure after the GRR repeat promotes the generation of p50 making it an acceptable substrate for the proteasome. This process is known as cotranslational processing. The processed form is active and the unprocessed form acts as an inhibitor (I kappa B-like), being able to form cytosolic complexes with NF-kappa B, trapping it in the cytoplasm. Complete folding of the region downstream of the GRR repeat precludes processing.,similarity:Contains 1 death domain.,similarity:Contains 1 RHD (Rel-like) domain.,similarity:Contains 7 ANK repeats.,subcellular location:Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B).,subunit:Component of the NF-kappa-B p65-p50 complex. Component of the NF-kappa-B p65-p50 complex. Homodimer; component of the NF-kappa-B p50-p50 complex. Component of the NF-kappa-B p105-p50 complex. Component of the NF-kappa-B p50-c-Rel complex. Component of a complex consisting of the NF-kappa-B p50-p50 homodimer and BCL3. Also interacts with MAP3K8. NF-kappa-B p50 subunit interacts with NCOA3 coactivator, which may coactivate NF-kappa-B dependent expression via its histone acetyltransferase activity. Interacts with DSIPI; this interaction prevents nuclear translocation and DNA-binding. Interacts with SPAG9 and UNC5CL. NFKB1/p105 interacts with CFLAR; the interaction inhibits p105 processing into p50. NFKB1/p105 forms a ternary complex with MAP3K8 and TNIP2. Interacts with GSK3B; the interaction prevents processing of p105 to p50. NFKB1/p50 interacts with NFKBIE. NFKB1/p50 interacts with NFKBIZ. Nuclear factor NF-kappa-B p50 subunit interacts with NFKBID., |
| 纯化 | Protein A |
| Clonality | Monoclonal |
| 修饰类型 | Unmodified |
| 细胞定位 | Cytoplasm, Nucleus |
| 组织表达 | Muscle,Rectum tumor,Uterus, |
| 研究领域 | >>Antifolate resistance;>>MAPK signaling pathway;>>Ras signaling pathway;>>cAMP signaling pathway;>>Chemokine signaling pathway;>>NF-kappa B signaling pathway;>>HIF-1 signaling pathway;>>Sphingolipid signaling pathway;>>PI3K-Akt signaling pathway;>>Apoptosis;>>Longevity regulating pathway;>>Cellular senescence;>>Osteoclast differentiation;>>Neutrophil extracellular trap formation;>>Toll-like receptor signaling pathway;>>NOD-like receptor signaling pathway;>>RIG-I-like receptor signaling pathway;>>Cytosolic DNA-sensing pathway;>>C-type lectin receptor signaling pathway;>>IL-17 signaling pathway;>>Th1 and Th2 cell differentiation;>>Th17 cell differentiation;>>T cell receptor signaling pathway;>>B cell receptor signaling pathway;>>TNF signaling pathway;>>Neurotrophin signaling pathway;>>Prolactin signaling pathway;>>Adipocytokine signaling pathway;>>Relaxin signaling pathway;>>Insulin resistance;>>Non-alcoholic fatty liver disease;>>AGE-RAGE signaling pathway in diabetic complications;>>Alcoholic liver disease;>>Alzheimer disease;>>Pathways of neurodegeneration - multiple diseases;>>Cocaine addiction;>>Epithelial cell signaling in Helicobacter pylori infection;>>Pathogenic Escherichia coli infection;>>Shigellosis;>>Salmonella infection;>>Pertussis;>>Legionellosis;>>Yersinia infection;>>Leishmaniasis;>>Chagas disease;>>Toxoplasmosis;>>Amoebiasis;>>Tuberculosis;>>Hepatitis C;>>Hepatitis B;>>Measles;>>Human cytomegalovirus infection;>>Influenza A;>>Human papillomavirus infection;>>Human T-cell leukemia virus 1 infection;>>Kaposi sarcoma-associated herpesvirus infection;>>Herpes simplex virus 1 infection;>>Epstein-Barr virus infection;>>Human immunodeficiency virus 1 infection;>>Coronavirus disease - COVID-19;>>Pathways in cancer;>>Transcriptional misregulation in cancer;>>Viral carcinogenesis;>>MicroRNAs in cancer;>>Chemical carcinogenesis - receptor activation;>>Chemical carcinogenesis - reactive oxygen species;>>Pancreatic cancer;>>Prostate cancer;>>Chronic myeloid leukemia;>>Acute myeloid leukemia;>>Small cell lung cancer;>>PD-L1 expression and PD-1 checkpoint pathway in cancer;>>Inflammatory bowel disease;>>Diabetic cardiomyopathy;>>Lipid and atherosclerosis;>>Fluid shear stress and atherosclerosis |
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