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Rabbit Anti-WNK4/PE-Cy7 Conjugated antibody (bs-0429R-PE-Cy7)
訂購熱線:400-901-9800
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bs-0429R-PE-Cy7
英文名稱 Rabbit Anti-WNK4/PE-Cy7 Conjugated antibody
中文名稱 PE-Cy7標(biāo)記的WNK4抗體
別    名 PHA 2B; PHA2B; PRKWNK 4; PRKWNK4; Protein kinase lysine deficient 4; Protein kinase with no lysine 4; Serine/threonine protein kinase WNK4; WNK lysine deficient protein kinase 4; WNK4_HUMAN.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領(lǐng)域 心血管  免疫學(xué)  激酶和磷酸酶  通道蛋白  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) Mouse,  (predicted: Human, Rat, )
產(chǎn)品應(yīng)用 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 135kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human WNK4
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(chǎn)品介紹 background:
Regulates the activity of the thiazide-sensitive Na-Cl cotransporter, SLC12A3, by phosphorylation which appears to prevent membrane trafficking of SLC12A3. Also inhibits the renal K(+)channel, KCNJ1, via a kinase-independent mechanism by which it induces clearance of the protein from the cell surface by clathrin-dependent endocytosis. WNK4 appears to act as a molecular switch that can vary the balance between NaCl reabsorption and K(+)secretion to maintain integrated homeostasis.

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, SGK1, TRPV5 and TRPV6. Regulates the activity of the thiazide-sensitive Na-Cl cotransporter, SLC12A3, by phosphorylation which appears to prevent membrane trafficking of SLC12A3. Also inhibits the renal K(+) channel, KCNJ1, via a kinase-independent mechanism by which it induces clearance of the protein from the cell surface by clathrin-dependent endocytosis. WNK4 appears to act as a molecular switch that can vary the balance between NaCl reabsorption and K(+) secretion to maintain integrated homeostasis. Phosphorylates NEDD4L.

Subunit:
Interacts with the C-terminal region of KCNJ1 (By similarity). Interacts with WNK1 and WNK3 (By similarity).

Subcellular Location:
Cell junction, tight junction (By similarity). Note=Present exclusively in intercellular junctions in the distal convoluted tubule and in both the cytoplasm and intercellular junctions in the cortical collecting duct. WNK4 is part of the tight junction complex (By similarity).

Tissue Specificity:
Expressed in kidney, colon and skin.

Post-translational modifications:
Phosphorylated by WNK1 and WNK3.

DISEASE:
Pseudohypoaldosteronism 2B (PHA2B) [MIM:614491]: An autosomal dominant disorder characterized by hypertension, hyperkalemia, hyperchloremia, mild hyperchloremic metabolic acidosis, and correction of physiologic abnormalities by thiazide diuretics. Note=The disease is caused by mutations affecting the gene represented in this entry.

Similarity:
Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. WNK subfamily.
Contains 1 protein kinase domain.

Database links:

Entrez Gene: 65266 Human

Omim: 601844 Human

SwissProt: Q96J92 Human

Unigene: 105448 Human



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

WNK4蛋白是一種新的絲氨酸/蘇氨酸激酶家族成員的基因,在遠(yuǎn)端腎小管表達(dá)(腎小管是腎臟的基本結(jié)構(gòu),在維持人體的水電解質(zhì)平衡方面有著重要的作用)而且,這一發(fā)現(xiàn)還有助于人們更好的了解腎臟的生理作用。
WNK4基因的發(fā)現(xiàn)是非常有意義的,WNK4的突變可能會引起高血壓病的發(fā)生,為人們研究血壓變化的發(fā)生機(jī)理提供了一個線索。
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