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GRK5 Protein, Human, Recombinant (His)

产品编号 TMPY-04555

G protein-coupled receptor kinase 5, also known as G protein-coupled receptor kinase GRK5 and GRK5, is a member of the protein kinase superfamily, AGC Ser/Thr protein kinase family, and GPRK subfamily. GRKs specifically phosphorylate agonist-occupied G protein-coupled receptors at the inner surface of the plasma membrane (PM), leading to receptor desensitization. GRKs utilize a variety of mechanisms to bind tightly, and sometimes reversibly, to cellular membranes. GRKs play an important role in mediating agonist-specific desensitization of numerous G protein-coupled receptors.GRK5 contains one AGC-kinase C-terminal domain, one protein kinase domain, and one RGS domain. GRK5 specifically phosphorylates the activated forms of G protein-coupled receptors. Phospholipid-stimulated autophosphorylation may represent a novel mechanism for membrane association and regulation of GRK5 activity. GRK5 deficiency significantly exaggerates microgliosis and astrogliosis in the presence of an inflammatory initiator, such as the excess fibrillar Abeta and the subsequent active inflammatory reactions. GRK5 deficiency has been linked to early Alzheimer's disease in humans and mouse models of the disease.

GRK5 Protein, Human, Recombinant (His)

GRK5 Protein, Human, Recombinant (His)

产品编号 TMPY-04555
G protein-coupled receptor kinase 5, also known as G protein-coupled receptor kinase GRK5 and GRK5, is a member of the protein kinase superfamily, AGC Ser/Thr protein kinase family, and GPRK subfamily. GRKs specifically phosphorylate agonist-occupied G protein-coupled receptors at the inner surface of the plasma membrane (PM), leading to receptor desensitization. GRKs utilize a variety of mechanisms to bind tightly, and sometimes reversibly, to cellular membranes. GRKs play an important role in mediating agonist-specific desensitization of numerous G protein-coupled receptors.GRK5 contains one AGC-kinase C-terminal domain, one protein kinase domain, and one RGS domain. GRK5 specifically phosphorylates the activated forms of G protein-coupled receptors. Phospholipid-stimulated autophosphorylation may represent a novel mechanism for membrane association and regulation of GRK5 activity. GRK5 deficiency significantly exaggerates microgliosis and astrogliosis in the presence of an inflammatory initiator, such as the excess fibrillar Abeta and the subsequent active inflammatory reactions. GRK5 deficiency has been linked to early Alzheimer's disease in humans and mouse models of the disease.
规格价格库存数量
50 μg¥ 2,5305日内发货
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产品信息

生物活性
No Kinase Activity
产品描述
G protein-coupled receptor kinase 5, also known as G protein-coupled receptor kinase GRK5 and GRK5, is a member of the protein kinase superfamily, AGC Ser/Thr protein kinase family, and GPRK subfamily. GRKs specifically phosphorylate agonist-occupied G protein-coupled receptors at the inner surface of the plasma membrane (PM), leading to receptor desensitization. GRKs utilize a variety of mechanisms to bind tightly, and sometimes reversibly, to cellular membranes. GRKs play an important role in mediating agonist-specific desensitization of numerous G protein-coupled receptors.GRK5 contains one AGC-kinase C-terminal domain, one protein kinase domain, and one RGS domain. GRK5 specifically phosphorylates the activated forms of G protein-coupled receptors. Phospholipid-stimulated autophosphorylation may represent a novel mechanism for membrane association and regulation of GRK5 activity. GRK5 deficiency significantly exaggerates microgliosis and astrogliosis in the presence of an inflammatory initiator, such as the excess fibrillar Abeta and the subsequent active inflammatory reactions. GRK5 deficiency has been linked to early Alzheimer's disease in humans and mouse models of the disease.
种属
Human
表达系统
Baculovirus Insect Cells
标签C-His
蛋白编号P34947
别名
GPRK5,G protein-coupled receptor kinase 5
蛋白构建
A DNA sequence encoding the human GRK5 (NP_005299.1) (Met 1-Ser 590) was fused with a polyhistidine tag at the C-terminus. Predicted N terminal: Met 1
蛋白纯度
> 90 % as determined by SDS-PAGE
分子量69 kDa (predicted); 58 kDa (reducing conditions)
内毒素< 1.0 EU/μg of the protein as determined by the LAL method.
缓冲液Lyophilized from a solution filtered through a 0.22 μm filter, containing 50 mM Tris, 100 mM NaCl, 0.5 mM PMSF, 1 mM DTT, 0.5 mM EDTA, 10% gly, pH 7.4. Typically, a mixture containing 5% to 8% trehalose, mannitol, and 0.01% Tween 80 is incorporated as a protective agent before lyophilization.
复溶方法
A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.
存储
It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
运输方式In general, Lyophilized powders are shipping with blue ice.
研究背景
G protein-coupled receptor kinase 5, also known as G protein-coupled receptor kinase GRK5 and GRK5, is a member of the protein kinase superfamily, AGC Ser/Thr protein kinase family, and GPRK subfamily. GRKs specifically phosphorylate agonist-occupied G protein-coupled receptors at the inner surface of the plasma membrane (PM), leading to receptor desensitization. GRKs utilize a variety of mechanisms to bind tightly, and sometimes reversibly, to cellular membranes. GRKs play an important role in mediating agonist-specific desensitization of numerous G protein-coupled receptors.GRK5 contains one AGC-kinase C-terminal domain, one protein kinase domain, and one RGS domain. GRK5 specifically phosphorylates the activated forms of G protein-coupled receptors. Phospholipid-stimulated autophosphorylation may represent a novel mechanism for membrane association and regulation of GRK5 activity. GRK5 deficiency significantly exaggerates microgliosis and astrogliosis in the presence of an inflammatory initiator, such as the excess fibrillar Abeta and the subsequent active inflammatory reactions. GRK5 deficiency has been linked to early Alzheimer's disease in humans and mouse models of the disease.

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