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MilliporeSigma
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PRS2437

Sigma-Aldrich

Anti-NOXA antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

Sinónimos:

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 Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

mouse, rat, human

technique(s)

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

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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

Immunogen

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

Linkage

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

Physical form

Solution in phosphate buffered saline containing 0.02% sodium azide

Disclaimer

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

10 - Combustible liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


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Greta Del Mistro et al.
NPJ systems biology and applications, 4, 39-39 (2018-11-13)
Metastatic melanoma remains a life-threatening disease because most tumors develop resistance to targeted kinase inhibitors thereby regaining tumorigenic capacity. We show the 2nd generation hexavalent TRAIL receptor-targeted agonist IZI1551 to induce pronounced apoptotic cell death in mutBRAF melanoma cells. Aiming
Taryn G Aubrecht et al.
Cell death & disease, 9(11), 1121-1121 (2018-11-08)
Traumatic brain injury (TBI) activates multiple neuronal cell death mechanisms, leading to post-traumatic neuronal loss and neurological deficits. TBI-induced cell cycle activation (CCA) in post-mitotic neurons causes regulated cell death involving cyclin-dependent kinase (CDK) activation and initiation of an E2F
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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