Anti-cdk5 (RABBIT) Antibody
CDK5 Antibody
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Host | Rabbit |
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Conjugate | Unconjugated |
Target Species | Human |
Reactivity | Rat, Human, Mouse |
Clonality | Polyclonal |
Application
| WB, IHC, E, IP, I, LCI |
Application Note | CDK5 antibody was tested by immunohistochemistry and immunoblot and found to be reactive against cdk5 (p31) at a dilution of 1:500 followed by reaction with Peroxidase conjugated Affinity Purified anti-Rabbit IgG [H&L] (Goat) code #611-1302. Anti-cdk5 (p31) is suitable for the detection by immunoblot of human, rat and mouse cdk5 (p31). Suggested dilutions for ELISA are 1:500 to 1:2000. |
Physical State | Liquid (sterile filtered) |
Immunogen | CDK5 (p31) peptide corresponding to the C-terminus of the human protein conjugated to Keyhole Limpet Hemocyanin (KLH). |
Preservative | 0.01% (w/v) Sodium Azide |
Gene ID | 1020 |
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Other Names | 1020 |
Purity | Anti-cdk5 was prepared from monospecific antiserum by delipidation and defibrination. Antiserum will specifically react with a 35 kDa cdk5 (p31) protein from human, rat and mouse tissue. No reaction was observed against other related cyclin dependent kinases. Cross reactivity with cdk5 (p31) from other species may also occur. |
Storage Condition | Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use. |
Precautions Note | This product is for research use only and is not intended for therapeutic or diagnostic applications. |
Name | CDK5 (HGNC:1774) |
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Function | 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. Negatively regulates the CACNA1B/CAV2.2 -mediated Ca(2+) release probability at hippocampal neuronal soma and synaptic terminals (By similarity). Activated by interaction with CDK5R1 (p35) and CDK5R2 (p39), especially in postmitotic 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-BMAL1 heterodimer in association with altered stability and subcellular distribution. |
Cellular Location | [Isoform 1]: Cytoplasm. Nucleus Cell membrane; Peripheral membrane protein. Perikaryon. Cell projection, lamellipodium {ECO:0000250|UniProtKB:P49615}. Cell projection, growth cone {ECO:0000250|UniProtKB:P49615}. Postsynaptic density {ECO:0000250|UniProtKB:Q03114}. Synapse {ECO:0000250|UniProtKB:Q03114} Note=In axonal growth cone with extension to the peripheral lamellipodia (By similarity). Under neurotoxic stress and neuronal injury conditions, CDK5R (p35) is cleaved by calpain to generate CDK5R1 (p25) in response to increased intracellular calcium. The elevated level of p25, when in complex with CDK5, leads to its subcellular misallocation as well as its hyperactivation. Colocalizes with CTNND2 in the cell body of neuronal cells, and with CTNNB1 in the cell-cell contacts and plasma membrane of undifferentiated and differentiated neuroblastoma cells. Reversibly attached to the plasma membrane in an inactive form when complexed to dephosphorylated p35 or CDK5R2 (p39), p35 phosphorylation releases this attachment and activates CDK5 |
Tissue Location | [Isoform 1]: Ubiquitously expressed (PubMed:17009320, PubMed:19693690). Accumulates in cortical neurons (at protein level) (PubMed:17009320). |
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Background
The protein encoded by the gene CDK5 is involved in the control of the cell cycle and interacts with D1 and D3-type G1 cyclins. CDK5 belongs to the protein kinase superfamily, the CMGC Ser/Thr protein kinase family and the CDC2/CDKX subfamily. CDK5 phosphorylates histone H1, tau, MAP2 and NF-H and NF-M and also interacts with p35 which activates the kinase. CDK5 forms a heterodimer, where CDK5 is the catalytic subunit and p35 is the regulatory subunit. CDK5 is also found in a trimolecular complex with CABLES1 and ABL1. CDK5 is a cytoplasmic protein.
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