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Rabbit Anti-GRK5/AP Conjugated antibody (bs-7540R-AP)
訂購熱線:400-901-9800
訂購郵箱:sales@bioss.com.cn
訂購QQ:  400-901-9800
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產品編號 bs-7540R-AP
英文名稱 Rabbit Anti-GRK5/AP Conjugated antibody
中文名稱 堿性磷酸酶(AP)標記的G蛋白偶聯受體激酶5抗體
別    名 G protein coupled receptor kinase 5; G protein coupled receptor kinase GRK5; G protein-coupled receptor kinase 5; G protein-coupled receptor kinase GRK5; GPRK5; GRK5; GRK5_HUMAN.  
規格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領域 心血管  細胞生物  信號轉導  轉錄調節因子  激酶和磷酸酶  G蛋白偶聯受體  G蛋白信號  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 (predicted: Human, Mouse, Rat, Dog, Pig, Cow, Horse, )
產品應用 WB=1:50-200 IHC-P=1:50-200 IHC-F=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 66kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human GRK5
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產品介紹 background:
This gene encodes a member of the guanine nucleotide-binding protein (G protein)-coupled receptor kinase subfamily of the Ser/Thr protein kinase family. The protein phosphorylates the activated forms of G protein-coupled receptors thus initiating their deactivation. It has also been shown to play a role in regulating the motility of polymorphonuclear leukocytes (PMNs). [provided by RefSeq, Jul 2008].

Function:
Serine/threonine kinase that phosphorylates preferentially the activated forms of a variety of G-protein-coupled receptors (GPCRs). Such receptor phosphorylation initiates beta-arrestin-mediated receptor desensitization, internalization, and signaling events leading to their down-regulation. Phosphorylates a variety of GPCRs, including adrenergic receptors, muscarinic acetylcholine receptors (more specifically Gi-coupled M2/M4 subtypes), dopamine receptors and opioid receptors. In addition to GPCRs, also phosphorylates various substrates: Hsc70-interacting protein/ST13, TP53/p53, HDAC5, and arrestin-1/ARRB1. Phosphorylation of ARRB1 by GRK5 inhibits G-protein independent MAPK1/MAPK3 signaling downstream of 5HT4-receptors. Phosphorylation of HDAC5, a repressor of myocyte enhancer factor 2 (MEF2) leading to nuclear export of HDAC5 and allowing MEF2-mediated transcription. Phosphorylation of TP53/p53, a crucial tumor suppressor, inhibits TP53/p53-mediated apoptosis. Phosphorylation of ST13 regulates internalization of the chemokine receptor. Phosphorylates rhodopsin (RHO) (in vitro) and a non G-protein-coupled receptor, LRP6 during Wnt signaling (in vitro).

Subunit:
Interacts with ST13 (via the C-terminus 303-319 AA). Interacts with TP53/p53. Interacts with HTR4 (via C-terminus 330-346 AA); this interaction is promoted by 5-HT (serotonin). Interacts with HDAC5.

Subcellular Location:
Cytoplasm. Nucleus. Cell membrane; Peripheral membrane protein. Note=Predominantly localized at the plasma membrane; targeted to the cell surface through the interaction with phospholipids. Nucleus localization is regulated in a GPCR and Ca(2+)/calmodulin-dependent fashion.

Tissue Specificity:
Highest levels in heart, placenta, lung, skeletal muscle, brain, liver, pancreas, kidney.

Post-translational modifications:
Autophosphorylated. Autophosphorylation may play a critical role in the regulation of GRK5 kinase activity.

Similarity:
Belongs to the protein kinase superfamily. AGC Ser/Thr protein kinase family. GPRK subfamily.
Contains 1 AGC-kinase C-terminal domain.
Contains 1 protein kinase domain.
Contains 1 RGS domain.

Database links:
UniProtKB/Swiss-Prot: P34947.1

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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