磷酸化赖氨酸缺陷型蛋白激酶1抗体

参考价:¥1
供货周期: 现货
品牌: GenWay
规格: 0.1ml/100μg和0.2ml/200μg等规格
货号:
CAS号:
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英文名称  Anti-Phospho-WNK1(Thr60)

中文名称  磷酸化赖氨酸缺陷型蛋白激酶1抗体

别    名  Erythrocyte 65 kDa protein; HSAN2; HSN2; hWNK1; KDP; KIAA0344; Kinase deficient protein; MGC163339; MGC163341; p65; PRKWNK1; Prostate derived sterile 20 like kinase; Protein kinase lysine deficient 1; Protein kinase lysine-deficient 1; Protein kinase with no lysine 1; PSK; Serine/threonine protein kinase WNK1; Serine/threonine-protein kinase WNK1; With no K; WNK lysine deficient protein kinase 1; WNK1; WNK1_HUMAN.

浓    度  1mg/1ml

规 格  0.1ml/100μg

抗体来源  Rabbit  

克隆类型  polyclonal

交叉反应  Human, Mouse, Rat, Chicken, Dog, Pig, Cow, Rabbit

产品类型  一抗  磷酸化抗体  

研究领域  细胞生物 信号转导 激酶和磷酸酶  

蛋白分子量  predicted molecular weight: 251kDa

性    状  Lyophilized or Liquid

磷酸化赖氨酸缺陷型蛋白激酶1抗体的主要功能是与抗原(包括外来的和自身的)相结合,从而有效地清除侵入机体内的微生物、寄生虫等异物,抗体(antibody)是一种应答抗原产生的、可与抗原特异性结合的蛋白质。每种抗体与特定的抗原决定基结合。这种结合可以使抗原失活,也可能无效但有时也会对机体造成病理性损害,如抗核抗体、抗双链DNA抗体、抗甲状腺球蛋白抗体等一些自身抗体的产生,对人体可造成危害。

免 疫 原  KLH conjugated Synthesised phosphopeptide derived from human WNK1 around the phosphorylation site of Thr60

亚    型  IgG

纯化方法  affinity purified by Protein A

储 存 液  0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide

产品应用   WB=1:100-500  ELISA=1:500-1000  IP=1:20-100  IHC-P=1:100-500  IHC-F=1:100-500  IF=1:100-500

(石蜡切片需做抗原修复)

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

保存条件  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.

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

产品介绍 WNK1 controls sodium and chloride ion transport by inhibiting the activity of WNK4, potentially by either phosphorylating the kinase or via an interaction between WNK4 and the autoinhibitory domain of WNK1. WNK4 regulates the activity of the thiazide sensitive Na/Cl cotransporter, SLC12A3, by phosphorylation. WNK1 may also play a role in actin cytoskeletal reorganization. WNK1 has 4 isoforms produced by alternative splicing. WNK1 is widely expressed, with highest levels observed in the testis, heart, kidney and skeletal muscle. Defects in WNK1 are a cause of pseudohypoaldosteronism type II (PHAII), an autosomal dominant disease characterized by severe hypertension, hyperkalemia, and sensitivity to thiazide diuretics which may result from a chloride shunt in the renal distal nephron.

Function : Serine/threonine kinase which plays an important role in the regulation of electrolyte homeostasis, cell signaling, survival, and proliferation. Acts as an activator and inhibitor of sodium-coupled chloride cotransporters and potassium-coupled chloride cotransporters respectively. Activates SCNN1A, SCNN1B, SCNN1D and SGK1. Controls sodium and chloride ion transport by inhibiting the activity of WNK4, by either phosphorylating the kinase or via an interaction between WNK4 and the autoinhibitory domain of WNK1. WNK4 regulates the activity of the thiazide-sensitive Na-Cl cotransporter, SLC12A3, by phosphorylation. WNK1 may also play a role in actin cytoskeletal reorganization. Phosphorylates NEDD4L (By similarity).

Subunit : Interacts with SYT2. Interacts with WNK3 and WNK4.

Subcellular Location : Cytoplasm.

Tissue Specificity : Widely expressed, with highest levels observed in the testis, heart, kidney and skeletal muscle. Isoform 3 is kidney-specific.

Post-translational modifications : O-glycosylated.

Phosphorylated upon DNA damage, probably by ATM or ATR.

DISEASE : Defects in WNK1 are a cause of pseudohypoaldosteronism type 2C (PHA2C) [MIM:614492]. An autosomal dominant disease characterized by severe hypertension, hyperkalemia, hyperchloremia, mild hyperchloremic metabolic acidosis in some cases, and correction of physiologic abnormalities by thiazide diuretics.

Defects in WNK1 are a cause of hereditary sensory and autonomic neuropathy type 2A (HSAN2A) [MIM:201300]. A form of hereditary sensory and autonomic neuropathy, a genetically and clinically heterogeneous group of disorders characterized by degeneration of dorsal root and autonomic ganglion cells, and by sensory and/or autonomic abnormalities. HSAN2A is an autosomal recessive disorder characterized by impairment of pain, temperature and touch sensation, onset of symptoms in infancy or early childhood, occurrence of distal extremity pathologies (paronychia, whitlows, ulcers, and Charcot joints), frequent amputations, sensory loss that affects all modalities of sensation (lower and upper limbs and perhaps the trunk as well), absence or diminution of tendon reflexes (usually in all limbs), minimal autonomic dysfunction, absence of sensory nerve action potentials, and virtual absence of myelinated fibers with decreased numbers of unmyelinated fibers in sural nerves.

磷酸化赖氨酸缺陷型蛋白激酶1抗体Similarity : Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. WNK subfamily.

Contains 1 protein kinase domain.

Database links : UniProtKB/Swiss-Prot: Q9H4A3.2


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