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瞬時(shí)受體電位離子通道蛋白4抗體（M亞家族）品牌 英文名稱  Anti-TRPM4

中文名稱  瞬時(shí)受體電位離子通道蛋白4抗體（M亞家族）品牌 

別    名 Long transient receptor potential channel 4; LTrpC-4; LTrpC4; Melastatin 4; Melastatin like 2 protein; Melastatin-4; Melastatin-like 2; Mls2s; PFHB1B; Transient receptor potential cation channel subfamily M member 4; Transient receptor potential cation channel, subfamily M, member 4; Trpm4; TRPM4_HUMAN; TRPM4B; 1110030C19Rik; AW047689; Calcium-activated non-selective cation channel 1; FLJ20041; hTRPM4.

產(chǎn)品屬性：

濃    度  1mg/1ml

規(guī) 格  0.2ml/200μg

抗體來源  Rabbit

克隆類型   polyclonal

交叉反應(yīng)   Human, Mouse, Rat

產(chǎn)品類型   一抗  

研究領(lǐng)域    細(xì)胞生物 免疫學(xué) 神經(jīng)生物學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 通道蛋白

蛋白分子量  predicted molecular weight: 134kDa 

性    狀   Lyophilized or Liquid

免 疫 原  KLH conjugated synthetic peptide derived from human TRPM4

亞    型  IgG

純化方法   affinity purified by Protein A

儲(chǔ) 存 液   Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4

瞬時(shí)受體電位離子通道蛋白4抗體（M亞家族）品牌 產(chǎn)品應(yīng)用   WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:50-200

（石蠟切片需做抗原修復(fù)） 

 not yet tested in other applications.

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

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. 

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

產(chǎn)品介紹 Calcium-activated non selective (CAN) cation channel that mediates membrane depolarization. While it is activated by increase in intracellular Ca(2+), it is impermeable to it. Mediates transport of monovalent cations (Na(+) > K(+) > Cs(+) > Li(+)), leading to depolarize the membrane. It thereby plays a central role in cadiomyocytes, neurons from entorhinal cortex, dorsal root and vomeronasal neurons, endocrine pancreas cells, kidney epithelial cells, cochlea hair cells etc. Participates in T-cell activation by modulating Ca(2+) oscillations after T lymphocyte activation, which is required for NFAT-dependent IL2 production. Involved in myogenic constriction of cerebral arteries. Controls insulin secretion in pancreatic beta-cells. May also be involved in pacemaking or could cause irregular electrical activity under conditions of Ca(2+) overload. Affects T-helper 1 (Th1) and T-helper 2 (Th2) cell motility and cytokine production through differential regulation of calcium signaling and NFATC1 localization. Enhances cell proliferation through up-regulation of the beta-catenin signaling pathway.

Involvement in disease:

Defects in TRPM4 are the cause of progressive familial heart block type 1B (PFHB1B) [MIM:604559]. It is a cardiac bundle branch disorder characterized by progressive alteration of cardiac conduction through the His-Purkinje system, with a pattern of a right bundle-branch block and/or left anterior hemiblock occurring individually or together. It leads to complete atrio-ventricular block causing syncope and sudden death.

Function : Calcium-activated non selective (CAN) cation channel that mediates membrane depolarization. While it is activated by increase in intracellular Ca(2+), it is impermeable to it. Mediates transport of monovalent cations (Na(+) > K(+) > Cs(+) > Li(+)), leading to depolarize the membrane. It thereby plays a central role in cadiomyocytes, neurons from entorhinal cortex, dorsal root and vomeronasal neurons, endocrine pancreas cells, kidney epithelial cells, cochlea hair cells etc. Participates in T-cell activation by modulating Ca(2+) oscillations after T lymphocyte activation, which is required for NFAT-dependent IL2 production. Involved in myogenic constriction of cerebral arteries. Controls insulin secretion in pancreatic beta-cells. May also be involved in pacemaking or could cause irregular electrical activity under conditions of Ca(2+) overload. Affects T-helper 1 (Th1) and T-helper 2 (Th2) cell motility and cytokine production through differential regulation of calcium signaling and NFATC1 localization. Enhances cell proliferation through up-regulation of the beta-catenin signaling pathway.

Subunit : Homomultimer.

Subcellular Location : Endoplasmic reticulum. Golgi apparatus and Cell membrane. Endoplasmic reticulum. Golgi apparatus

Tissue Specificity : Widely expressed with a high expression in intestine and prostate. In brain, it is both expressed in whole cerebral arteries and isolated vascular smooth muscle cells. Prominently expressed in Purkinje fibers. Expressed at higher levels in T-helper 2 (Th2) cells as compared to T-helper 1 (Th1) cells.

Post-translational modifications : Phosphorylation by PKC leads to increase the sensitivity to Ca(2+).

Sumoylated. Desumoylated by SENP1.

DISEASE : Defects in TRPM4 are the cause of progressive familial heart block type 1B (PFHB1B) [MIM:604559]. It is a cardiac bundle branch disorder characterized by progressive alteration of cardiac conduction through the His-Purkinje system, with a pattern of a right bundle-branch block and/or left anterior hemiblock occurring individually or together. It leads to complete atrioventricular block causing syncope and sudden death.

Similarity : Belongs to the transient receptor (TC 1.A.4) family. LTrpC subfamily. TRPM4 sub-subfamily.

Database links :

Entrez Gene: 54795 Human

Entrez Gene: 68667 Mouse

Entrez Gene: 171143 Rat

Omim: 606936 Human

SwissProt: Q8TD43 Human

SwissProt: Q7TN37 Mouse

SwissProt: Q9ESQ5 Rat

Unigene: 467101 Human

Unigene: 439890 Mouse

Unigene: 205004 Rat

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