Phospho-IL-10R alpha (Tyr496) Antibody - #AF3435
产品: | 磷酸化 IL-10R alpha (Tyr496) 抗体 |
货号: | AF3435 |
描述: | Rabbit polyclonal antibody to Phospho-IL-10R alpha (Tyr496) |
应用: | WB IF/ICC |
反应: | Human |
预测: | Pig, Horse, Rabbit, Dog, Chicken |
分子量: | 63kDa; 63kD(Calculated). |
蛋白号: | Q13651 |
RRID: | AB_2834877 |
产品描述
*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.
引用格式: Affinity Biosciences Cat# AF3435, RRID:AB_2834877.
展开/折叠
CD210; CDw210a; CDw210a antigen; HIL 10R; HIL10R; I10R1_HUMAN; IL 10R 1; IL 10R A; IL 10R; IL 10R1; IL-10 receptor subunit alpha; IL-10R subunit 1; IL-10R subunit alpha; IL-10R1; IL-10RA; IL10R; IL10R1; IL10RA; Interleukin 10 receptor alpha; Interleukin 10 receptor alpha chain; Interleukin-10 receptor subunit 1; Interleukin-10 receptor subunit alpha;
抗原和靶标
Primarily expressed in hematopoetic cells including B-cells, T-cells, NK cells, monocytes and macrophages. Not expressed in non-hematopoetic cells such as fibroblasts or endothelial cells.
- Q13651 I10R1_HUMAN:
- Protein BLAST With
- NCBI/
- ExPASy/
- Uniprot
MLPCLVVLLAALLSLRLGSDAHGTELPSPPSVWFEAEFFHHILHWTPIPNQSESTCYEVALLRYGIESWNSISNCSQTLSYDLTAVTLDLYHSNGYRARVRAVDGSRHSNWTVTNTRFSVDEVTLTVGSVNLEIHNGFILGKIQLPRPKMAPANDTYESIFSHFREYEIAIRKVPGNFTFTHKKVKHENFSLLTSGEVGEFCVQVKPSVASRSNKGMWSKEECISLTRQYFTVTNVIIFFAFVLLLSGALAYCLALQLYVRRRKKLPSVLLFKKPSPFIFISQRPSPETQDTIHPLDEEAFLKVSPELKNLDLHGSTDSGFGSTKPSLQTEEPQFLLPDPHPQADRTLGNREPPVLGDSCSSGSSNSTDSGICLQEPSLSPSTGPTWEQQVGSNSRGQDDSGIDLVQNSEGRAGDTQGGSALGHHSPPEPEVPGEEDPAAVAFQGYLRQTRCAEEKATKTGCLEEESPLTDGLGPKFGRCLVDEAGLHPPALAKGYLKQDPLEMTLASSGAPTGQWNQPTEEWSLLALSSCSDLGISDWSFAHDLAPLGCVAAPGGLLGSFNSDLVTLPLISSLQSSE
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。
High(score>80) Medium(80>score>50) Low(score<50) No confidence
翻译修饰 - Q13651 作为底物
研究背景
Cell surface receptor for the cytokine IL10 that participates in IL10-mediated anti-inflammatory functions, limiting excessive tissue disruption caused by inflammation. Upon binding to IL10, induces a conformational change in IL10RB, allowing IL10RB to bind IL10 as well. In turn, the heterotetrameric assembly complex, composed of two subunits of IL10RA and IL10RB, activates the kinases JAK1 and TYK2 that are constitutively associated with IL10RA and IL10RB respectively. These kinases then phosphorylate specific tyrosine residues in the intracellular domain in IL10RA leading to the recruitment and subsequent phosphorylation of STAT3. Once phosphorylated, STAT3 homodimerizes, translocates to the nucleus and activates the expression of anti-inflammatory genes. In addition, IL10RA-mediated activation of STAT3 inhibits starvation-induced autophagy.
Phosphorylated. Phosphorylation of the cytoplasmic tail induced STAT3 activation.
Ubiquitinated by BTRC; ubiquitination leads to endocytosis and subsequent degradation of IL10RA.
Cell membrane>Single-pass type I membrane protein. Cytoplasm.
Primarily expressed in hematopoetic cells including B-cells, T-cells, NK cells, monocytes and macrophages. Not expressed in non-hematopoetic cells such as fibroblasts or endothelial cells.
Interacts with IL10. Interacts with IL10RB. Interacts (via its cytoplasmic domain) with JAK1 (via N-terminus). Interacts with BTRC; this interaction leads to IL10RA ubiquitination and subsequent degradation. Interacts with STAT3 (By similarity).
(Microbial infection) Interacts with human cytomegalovirus protein IL10.
(Microbial infection) Interacts with Epstein-Barr virus protein IL10.
Belongs to the type II cytokine receptor family.
研究领域
· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction. (View pathway)
· Environmental Information Processing > Signal transduction > Jak-STAT signaling pathway. (View pathway)
· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.
· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.
· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.
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