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Merck
모든 사진(3)

주요 문서

PRS2437

Sigma-Aldrich

Anti-NOXA antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

동의어(들):

Anti-APR, Anti-PMA-induced protein 1, Anti-PMAIP1, Anti-Phorbol-12-myristate-13-acetate-induced protein 1

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About This Item

MDL number:
UNSPSC 코드:
12352203
NACRES:
NA.41

생물학적 소스

rabbit

Quality Level

결합

unconjugated

항체 형태

affinity isolated antibody

항체 생산 유형

primary antibodies

클론

polyclonal

양식

buffered aqueous solution

종 반응성

mouse, rat, human

기술

immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable

UniProt 수납 번호

배송 상태

dry ice

저장 온도

−20°C

타겟 번역 후 변형

unmodified

유전자 정보

human ... PMAIP1(5366)
mouse ... Pmaip1(58801)

면역원

a synthetic peptide corresponding to 17 amino acids at the amino-terminus of mouse Noxa.

결합

The action of this antibody can be blocked using blocking peptide SBP2437.

물리적 형태

Solution in phosphate buffered saline containing 0.02% sodium azide

면책조항

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.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


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문서 라이브러리 방문

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Yelin Chen et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(46), 15327-15339 (2014-11-14)
Neuronal gene expression is modulated by activity via calcium-permeable receptors such as NMDA receptors (NMDARs). While gene expression changes downstream of evoked NMDAR activity have been well studied, much less is known about gene expression changes that occur under conditions
Hou-Zao Chen et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(36), 11897-11912 (2014-09-05)
The failure of past efforts to develop effective stroke treatments is at least partially because these treatments often interfered with essential physiological functions, even though they are targeted toward pathophysiological events, such as inflammation, excitotoxicity, and oxidative stress. Thus, the

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