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安全信息

AV37192

Sigma-Aldrich

Anti-SP1 (AB1) antibody produced in rabbit

IgG fraction of antiserum

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NACRES:
NA.41

生物来源

rabbit

质量水平

100

偶联物

unconjugated

抗体形式

IgG fraction of antiserum

antibody product type

primary antibodies

克隆

polyclonal

形式

buffered aqueous solution

分子量

51 kDa

species reactivity

human, mouse, rat

浓度

0.5 mg - 1 mg/mL

technique(s)

western blot: suitable

NCBI登记号

NP_038700

UniProt登记号

O89090-2

运输

wet ice

储存温度

−20°C

target post-translational modification

unmodified

Gene Information

mouse ... SP1(20683)

免疫原

Synthetic peptide directed towards the middle region of human SP1

生化/生理作用

SP1 is a transcription factor binds to GC box

序列

Synthetic peptide located within the following region: GSSGTSSQGQTPQRVGGLQGSDSLNIQQNQTSGGSLQGSQQKEGEQSQQT

外形

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

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.

储存分类代码

10 - Combustible liquids

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

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Hemanth N Banavath et al.
Journal of the American Heart Association, 8(24), e012919-e012919 (2019-12-06)
Background Translocation of miR-181c into cardiac mitochondria downregulates the mitochondrial gene, mt-COX1. miR-181c/d-/- hearts experience less oxidative stress during ischemia/reperfusion (I/R) and are protected against I/R injury. Additionally, miR-181c overexpression can increase mitochondrial matrix Ca2+ ([Ca2+]m), but the mechanism by
Barbara Roman et al.
Journal of molecular and cellular cardiology, 144, 87-96 (2020-05-23)
In cardiomyocytes, there is microRNA (miR) in the mitochondria that originates from the nuclear genome and matures in the cytoplasm before translocating into the mitochondria. Overexpression of one such miR, miR-181c, can lead to heart failure by stimulating reactive oxygen

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