CDK5 anticorps (pTyr15)

N° du produit ABIN6255818

Cet anticorps Lapin Polyclonal détecte spécifiquement CDK5 dans WB, ELISA, IF et ICC. Il présente une réactivité envers Humain, Souris, Rat et Singe.

Aperçu rapide pour CDK5 anticorps (pTyr15) (ABIN6255818)

Antigène: CDK5 (Cyclin-Dependent Kinase 5 (CDK5))

Reactivité: Humain, Souris, Rat, Singe

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp CDK5 est non-conjugé

Application: Western Blotting (WB), ELISA, Immunofluorescence (IF), Immunocytochemistry (ICC)

Détail du produit anti-CDK5 anticorps

Épitope: pTyr15

Specificité: Phospho-CDK5 (Tyr15) Antibody detects endogenous levels of CDK5 only when phosphorylated at Tyrosine 15

Réactivité croisée: Humain, Singe, Souris, Rat (Rattus)

Purification: The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho- and non-phospho-peptide affinity columns.

Immunogène: A synthesized peptide derived from human CDK5 around the phosphorylation site of Tyrosine 15

Isotype: IgG

Information d'application

Indications d'application: WB 1:500-1:2000, IF/ICC 1:100-1:500

Restrictions: For Research Use only

Stockage

Format: Liquid

Concentration: 1 mg/mL

Buffer: Rabbit IgG in phosphate buffered saline ,  pH 7.4, 150  mM NaCl, 0.02 % sodium azide and 50 % glycerol.

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Stock: -20 °C

Stockage commentaire: Store at -20 °C.Stable for 12 months from date of receipt

Date de péremption: 12 months

Détails sur CDK5

Antigène: CDK5 (Cyclin-Dependent Kinase 5 (CDK5))

Autre désignation: CDK5

Sujet:

Description: Proline-directed serine/threonine-protein kinase essential for neuronal cell cycle arrest and differentiation and may be involved in apoptotic cell death in neuronal diseases by triggering abortive cell cycle re-entry. Interacts with D1 and D3-type G1 cyclins. Phosphorylates SRC, NOS3, VIM/vimentin, p35/CDK5R1, MEF2A, SIPA1L1, SH3GLB1, PXN, PAK1, MCAM/MUC18, SEPT5, SYN1, DNM1, AMPH, SYNJ1, CDK16, RAC1, RHOA, CDC42, TONEBP/NFAT5, MAPT/TAU, MAP1B, histone H1, p53/TP53, HDAC1, APEX1, PTK2/FAK1, huntingtin/HTT, ATM, MAP2, NEFH and NEFM. Regulates several neuronal development and physiological processes including neuronal survival, migration and differentiation, axonal and neurite growth, synaptogenesis, oligodendrocyte differentiation, synaptic plasticity and neurotransmission, by phosphorylating key proteins. Activated by interaction with CDK5R1 (p35) and CDK5R2 (p39), especially in post-mitotic neurons, and promotes CDK5R1 (p35) expression in an autostimulation loop. Phosphorylates many downstream substrates such as Rho and Ras family small GTPases (e.g. PAK1, RAC1, RHOA, CDC42) or microtubule-binding proteins (e.g. MAPT/TAU, MAP2, MAP1B), and modulates actin dynamics to regulate neurite growth and/or spine morphogenesis. Phosphorylates also exocytosis associated proteins such as MCAM/MUC18, SEPT5, SYN1, and CDK16/PCTAIRE1 as well as endocytosis associated proteins such as DNM1, AMPH and SYNJ1 at synaptic terminals. In the mature central nervous system (CNS), regulates neurotransmitter movements by phosphorylating substrates associated with neurotransmitter release and synapse plasticity, synaptic vesicle exocytosis, vesicles fusion with the presynaptic membrane, and endocytosis. Promotes cell survival by activating anti-apoptotic proteins BCL2 and STAT3, and negatively regulating of JNK3/MAPK10 activity. Phosphorylation of p53/TP53 in response to genotoxic and oxidative stresses enhances its stabilization by preventing ubiquitin ligase-mediated proteasomal degradation, and induces transactivation of p53/TP53 target genes, thus regulating apoptosis. Phosphorylation of p35/CDK5R1 enhances its stabilization by preventing calpain-mediated proteolysis producing p25/CDK5R1 and avoiding ubiquitin ligase-mediated proteasomal degradation. During aberrant cell-cycle activity and DNA damage, p25/CDK5 activity elicits cell-cycle activity and double-strand DNA breaks that precedes neuronal death by deregulating HDAC1. DNA damage triggered phosphorylation of huntingtin/HTT in nuclei of neurons protects neurons against polyglutamine expansion as well as DNA damage mediated toxicity. Phosphorylation of PXN reduces its interaction with PTK2/FAK1 in matrix-cell focal adhesions (MCFA) during oligodendrocytes (OLs) differentiation. Negative regulator of Wnt/beta-catenin signaling pathway. Activator of the GAIT (IFN-gamma-activated inhibitor of translation) pathway, which suppresses expression of a post-transcriptional regulon of proinflammatory genes in myeloid cells, phosphorylates the linker domain of glutamyl-prolyl tRNA synthetase (EPRS) in a IFN-gamma-dependent manner, the initial event in assembly of the GAIT complex. Phosphorylation of SH3GLB1 is required for autophagy induction in starved neurons. Phosphorylation of TONEBP/NFAT5 in response to osmotic stress mediates its rapid nuclear localization. MEF2 is inactivated by phosphorylation in nucleus in response to neurotoxin, thus leading to neuronal apoptosis. APEX1 AP-endodeoxyribonuclease is repressed by phosphorylation, resulting in accumulation of DNA damage and contributing to neuronal death. NOS3 phosphorylation down regulates NOS3-derived nitrite (NO) levels. SRC phosphorylation mediates its ubiquitin-dependent degradation and thus leads to cytoskeletal reorganization. May regulate endothelial cell migration and angiogenesis via the modulation of lamellipodia formation. Involved in dendritic spine morphogenesis by mediating the EFNA1-EPHA4 signaling. The complex p35/CDK5 participates in the regulation of the circadian clock by modulating the function of CLOCK protein: phosphorylates CLOCK at 'Thr-451' and 'Thr-461' and regulates the transcriptional activity of the CLOCK-ARNTL/BMAL1 heterodimer in association with altered stability and subcellular distribution.

Gene: CDK5

Poids moléculaire: 33kDa

ID gène: 1020

UniProt: Q00535

Pathways: Cycle Cellulaire, Regulation of Muscle Cell Differentiation, Synaptic Membrane, Regulation of Cell Size, Skeletal Muscle Fiber Development, Synaptic Vesicle Exocytosis