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Rabbit Anti-SLC12A3/Gold Conjugated antibody (bs-7694R-Gold)
訂購(gòu)熱線:400-901-9800
訂購(gòu)郵箱:sales@m.p2b3.cn
訂購(gòu)QQ:  400-901-9800
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說(shuō) 明 書: 100ul(10nm  15nm  35nm
100ul/2980.00元
大包裝/詢價(jià)
產(chǎn)品編號(hào) bs-7694R-Gold
英文名稱 Rabbit Anti-SLC12A3/Gold Conjugated antibody
中文名稱 膠體金標(biāo)記的鈉氯離子轉(zhuǎn)運(yùn)蛋白抗體
別    名 Na Cl symporter; Na-Cl symporter; NaCl electroneutral thiazide sensitive cotransporter; NCCT; S12A3_HUMAN; slc12a3; Solute carrier family 12 (sodium/chloride transporters) member 3; Solute carrier family 12 member 3; Thiazide sensitive Na Cl cotransporter; Thiazide sensitive sodium chloride cotransporter; Thiazide-sensitive sodium-chloride cotransporter; TSC.  
規(guī)格價(jià)格 100ul/2980元 購(gòu)買        大包裝/詢價(jià)
說(shuō) 明 書 100ul(10nm  15nm  35nm
研究領(lǐng)域 腫瘤  心血管  細(xì)胞生物  通道蛋白  轉(zhuǎn)運(yùn)蛋白  
抗體來(lái)源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) (predicted: Human, Mouse, Rat, Dog, Cow, Rabbit, )
產(chǎn)品應(yīng)用 IEM=1:20-200 ICA=1:20-200 ChIP=1:20-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 113kDa
性    狀 Lyophilized or Liquid
濃    度 0.4mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human SLC12A3/NCCT
亞    型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 存 液 0.02M TBS(pH8.2) with 1% BSA, 0.03% Proclin300.
保存條件 Store at 2-8 oC for 3-6 months. Avoid repeated freeze/thaw cycles.
產(chǎn)品介紹 background:
Na-K-Cl cotransporters (NKCC) are channel proteins that aid in the transcellular movement of chloride across both secretory and absorptive epithelia. NKCC1 is expressed in muscle cells, neurons, and red blood cells. In the basolateral membrane of secretory epithelia, NKCC1 mediates active chloride secretion. The gene encoding human NKCC1 maps to chromosome 5q23.3. In mice, disruption of the NKCC1 gene leads to deafness and impaired balance. NKCC2 is specifically expressed in the kidney where it mediates active reabsorption of sodium chloride in the thick ascending limb of the loop of Henle. NKCC2 is sensitive to the clinically important diuretics furosemide and bumetanide. The gene encoding human NKCC2 maps to chromosome 15q15-q21 and mutations in this gene lead to Bartter’s syndrome, an inherited hypokalaemic alkalosis. NCCT is a thiazide-sensitive Na-Cl cotransporter that is primarily expressed in the distal convoluted tubule of the kidney where it accounts for a significant fraction of net renal sodium reabsorption. The gene for human NCCT map to chromosome 16q13. Mutations in the gene encoding NCCT cause Gitelman’s syndrome, a subset of Bartter’s syndrome.

Function:
Electrically silent transporter system. Mediates sodium and chloride reabsorption.

Subunit:
Interacts with KLHL3.

Subcellular Location:
Membrane.

Tissue Specificity:
Predominant in kidney.

Post-translational modifications:
Ubiquitinated; ubiquitination is essential for regulation of endocytosis (By similarity). May be ubiquitinated by the BCR(KLHL3) complex.

DISEASE:
Defects in SLC12A3 are the cause of Gitelman syndrome (GS). GS is an autosomal recessive disorder characterized by hypokalemic alkalosis in combination with hypomagnesemia, low urinary calcium, and increased renin activity associated with normal blood pressure. Patients are often asymptomatic or present transient periods of muscular weakness and tetany, usually accompanied by abdominal pain, vomiting and fever. The phenotype is highly heterogeneous in terms of age at onset and severity. Cardinal features such as hypocalciuria and hypomagnesemia might also change during the life cycle of a given patient. GS has overlapping features with Bartter syndrome.

Similarity:
Belongs to the SLC12A transporter family.

Database links:

Entrez Gene: 6559 Human

Entrez Gene: 20497 Mouse

Entrez Gene: 54300 Rat

Omim: 600968 Human

SwissProt: P55017 Human

SwissProt: P59158 Mouse

SwissProt: P55018 Rat

Unigene: 669115 Human

Unigene: 25804 Mouse

Unigene: 10467 Rat



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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