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P9489

Sigma-Aldrich

Anti-p35 (Cdk5 Regulator) antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonyme(s) :

Anti-CDK5P35, Anti-CDK5R, Anti-NCK5A, Anti-p23, Anti-p25, Anti-p35, Anti-p35nck5a

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About This Item

Numéro MDL:
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.46

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

IgG fraction of antiserum

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 35 kDa

Espèces réactives

human, rat

Technique(s)

microarray: suitable
western blot: 1:1,000 using a rat brain extract (cytosolic fraction)

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

Description générale

Cell division protein kinase 5 (Cdk5) is a serine/threonine kinase and shares homology to other Cdks. It belongs to cdk family.

Immunogène

synthetic peptide corresponding to the C-terminus of p35 (Cdk5R), (human, amino acids 192-209).

Application

Anti-p35 (Cdk5 Regulator) antibody produced in rabbit has been used in western blotting and immunohistochemistry.

Actions biochimiques/physiologiques

Cell division protein kinase 5 (Cdk5) kinase activity can be detected mainly in postmitotic neurons in the central nervous system (CNS). Cdk5/p35 activity is required in the mature CNS. Cdk5 phosphorylates dopamine and cyclic adenosine 3′,5′-monophosphate-regulated phosphoprotein of 32 kDa (DARPP-32) and Syntaxin-binding protein 1 (Munc18), which in turn affects synaptic vesicle endocytosis. Deregulation of Cdk5 activity contributes to the pathogenesis of neurodegenerative diseases such as Alzheimer′s disease (AD). It mediates neuronal migration during cortical development. Cdk5-/- mice exhibit embryonic lethality associated with disruption of the cortical laminar structures in the cerebral cortex, olfactory bulb, hippocampus, and cerebellar cortex. Mice lacking p35 display defects in cortical lamination and fasciculation of axonal fibers. In developing mice brain, Cdk5/p35 interacts with Reelin/Dab1 and positions of cortical neurons.

Forme physique

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Clause de non-responsabilité

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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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

Deregulated Cdk5 activity is involved in inducing Alzheimer?s disease
Shukla V, et al.
Archives of Medical Research, 43(8), 655-662 (2012)
Cyclin-dependent kinase 5 associated with p39 promotes Munc18-1 phosphorylation and Ca2+-dependent exocytosis
Lilja L, et al.
The Journal of Biological Chemistry, 279(28), 29534-29541 (2004)
NGF controls APP cleavage by downregulating APP phosphorylation at Thr668: relevance for Alzheimer's disease
Triaca V, et al.
Aging Cell, 15(4), 661-672 (2016)
Regulation of N-cadherin-mediated adhesion by the p35-Cdk5 kinase
Kwon YT, et al.
Current Biology, 10(7), 363-372 (2000)
Perinatal abrogation of Cdk5 expression in brain results in neuronal migration defects
Hirasawa M, et al.
Proceedings of the National Academy of Sciences of the USA, 101(16), 6249-6254 (2004)

Articles

Alzheimer's disease (AD) is the most common cause of dementia in the elderly and is characterized by gradual loss of cognitive functions.

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