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Merck
CN

C7492

Sigma-Aldrich

Monoclonal Anti-Calreticulin antibody produced in mouse

clone TO-11, tissue culture supernatant, buffered aqueous solution

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别名:
Calreticulin Antibody Flow Cytometry, Anti-Autoantigen Ro
UNSPSC代码:
12352203
NACRES:
NA.44

生物来源

mouse

质量水平

偶联物

unconjugated

抗体形式

tissue culture supernatant

抗体产品类型

primary antibodies

克隆

TO-11, monoclonal

形式

buffered aqueous solution

分子量

antigen ~50 kDa

种属反应性

human

技术

flow cytometry: suitable
immunocytochemistry: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: 1:50-1:100 using total cell extract of HeLa cells

同位素/亚型

IgG1

UniProt登记号

运输

dry ice

储存温度

−20°C

靶向翻译后修饰

unmodified

基因信息

human ... CALR(811)

一般描述

Monoclonal Anti-Calreticulin (mouse IgG1 isotype) is derived from the hybridoma TO-11 produced by the fusion of mouse myeloma cells (P3-X63-AG8.653 cells) and splenocytes from BALB/c mice.
Monoclonal Anti-Calreticulin (mouse IgG1 isotype) is derived from the hybridoma TO-11 produced by the fusion of mouse myeloma cells (P3-X63-AG8.653 cells) and splenocytes from BALB/c mice. Calreticulin is a molecular chaperones in endoplasmic reticulum lumen. Calreticulin acts as a lectin-like chaperone binding oligosaccharide residues of newly synthesized N-linked glycoproteins, and misfolded proteins. Calreticulin is a protein binding Ca2+ ions. It is encoded by the CALR gene in humans.

应用

Monoclonal Anti-Calreticulin antibody produced in mouse is suitable for the following applications:
  • Flow cytometry
  • Immunocytochemistry
  • Immunohistochemistry
  • Indirect ELISA
  • Western blotting

生化/生理作用

Calreticulin and Its variants causes differential effects on thrombopoiesis. Somatic mutations of calreticulin (CALR) gene causes thrombocythemia (ET) and primary myelofibrosis (PMF).
It is believed to play a critical role in quality control processes during protein synthesis and folding. Increased expression of calreticulin increases Ca2+ storage capacity of the ER. It also appears to modulate store-operated Ca2+ -influx, and to alter Ca2+ transport by the sarcoplasmic/ER Ca2+ -ATPase (SERCA). Overexpression of calreticulin results in increased sensitivity of HeLa cells to drug-induced apoptosis. In contrast, calreticulin-deficient cells show increased resistance to apoptosis. Calreticulin gene disruption leads toimpairment of cardiac development. Loss of calreticulin function favors ubiquitin-proteosome activity. It plays a critical role in Ca2+ homeostasis.

外形

Culture supernatant solution containing 15 mM sodium azide.

免责声明

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)

法规信息

常规特殊物品

分析证书(COA)

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Enhanced ubiquitin-proteasome activity in calreticulin deficient cells: a compensatory mechanism for cell survival
Uvarov AVand Mesaeli N
Biochimica et Biophysica Acta, 1783(6), 1237-1247 (2008)
Calnexin and calreticulin, molecular chaperones of the endoplasmic reticulum
Calreticulin, 49-62 (2003)
Calreticulin, a Ca2+-binding chaperone of the endoplasmic reticulum
Gelebart P, et al.
The International Journal of Biochemistry & Cell Biology, 37(2), 260-266 (2005)
Ayalew Tefferi et al.
American journal of hematology, 89(8), E121-E124 (2014-04-23)
CALR (calreticulin) trails JAK2 as the second most mutated gene in essential thrombocythemia (ET). Mutant CALR in ET is a result of frameshift mutations, caused by exon 9 deletions or insertions; type-1, 52-bp deletion (p.L367fs*46), and type-2, 5-bp TTGTC insertion
Irradiation enhances the therapeutic effect of the oncolytic adenovirus XVir-N-31 in brain tumor initiating cells
Czolk R, et al.
International Journal of Molecular Medicine (2019)

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