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Rabbit Anti-TRPM4/Gold Conjugated antibody (bs-9051R-Gold)
訂購熱線:400-901-9800
訂購郵箱:sales@bioss.com.cn
訂購QQ:  400-901-9800
技術(shù)支持:techsupport@bioss.com.cn
說 明 書: 100ul(10nm  15nm  35nm
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bs-9051R-Gold
英文名稱 Rabbit Anti-TRPM4/Gold Conjugated antibody
中文名稱 膠體金標(biāo)記的瞬時受體電位離子通道蛋白4抗體(M亞家族)
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.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul(10nm  15nm  35nm
研究領(lǐng)域 細(xì)胞生物  免疫學(xué)  神經(jīng)生物學(xué)  信號轉(zhuǎn)導(dǎo)  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 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 134kDa
性    狀 Lyophilized or Liquid
濃    度 0.4mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human TRPM4
亞    型 IgG
純化方法 affinity purified by Protein A
儲 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:
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



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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