Anti-CDK5 Antibody Picoband®

Overview

Anti-CDK5 Antibody Picoband® is an antibody for CDK5 detection raised in Rabbit (Polyclonal, Rabbit IgG), with reported reactivity: Human,Mouse,Rat. Commonly used in WB, IHC, Flow Cytometry, ELISA workflows.

Key elements and design rationale

• Target: CDK5 (cyclin-dependent kinase 5); UniProt: Q00535
• Antibody format: Rabbit, Polyclonal, Rabbit IgG
• Molecular weight: 33 kDa, calculated 40108 MW
• Applications: WB, IHC, Flow Cytometry, ELISA

Vendor description (summary): Boster Bio Anti-CDK5 Antibody Picoband® catalog # A00511-1.

Biological background

Biological context: Proline-ed 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.

Expression and localization notes: cellular localization: Cell membrane. Peripheral membrane protein. Postsynaptic density. Cytoplasm. Perikaryon. Lamellipodium. Growth cone., tissue context: Isoform 1 is ubiquitously expressed. Accumulates in cortical neurons (at protein level). Isoform 2 has only been detected in testis, skeletal muscle, colon, bone marrow and ovary..

Common research applications

• Western blotting (WB): Compare CDK5 levels across samples and conditions using appropriate loading and biological controls.
• Immunohistochemistry (IHC): Evaluate spatial distribution of CDK5 in tissue sections, considering fixation and antigen retrieval effects.
• Flow cytometry: Quantify CDK5-positive populations in single-cell suspensions with appropriate gating and controls.
• ELISA: Use antibody-based detection formats to assess antigen presence or binding in plate-based assays.

Notes for experimental interpretation

• Account for isoforms, post-translational modifications, and sample-specific processing that can shift apparent molecular weight or epitope accessibility.
• Use positive/negative biological controls where possible (e.g., known-expressing cells/tissues, knockdown/knockout models) and include appropriate secondary-only/isotype controls for imaging workflows.

Additional product notes (from provided fields)

• Specificity: No cross reactivity with other proteins.
• Background: CDK5, Cyclin-Dependent Kinase5, is also known as PSSALRE. The p34 (CDC2) protein kinase regulates important transitions in the eukaryotic cell cycle.The PSSALRE expression is in all human tissues and cell lines tested.The the CDK5 gene is mapped to chromosome 7q36. Cyclin-dependent kinase-5 is predominantly expressed in neurons where it phosphorylates both high molecular weight neurofilaments and microtubule-associated protein tau. CDK5 is required for proper development of the mammalian central nervous system. To be activated, CDK5 must associate with its regulatory subunit, p35 (CDK5R1). CDK5 can phosphorylate DARPP32 at threonine-75, converting it into an inhibitor of PKA.
• Cross reactivity: No cross-reactivity with other proteins.
• Cellular localization: Cell membrane. Peripheral membrane protein. Postsynaptic density. Cytoplasm. Perikaryon. Lamellipodium. Growth cone.
• Tissue details: Isoform 1 is ubiquitously expressed. Accumulates in cortical neurons (at protein level). Isoform 2 has only been detected in testis, skeletal muscle, colon, bone marrow and ovary.
• Research category: Cofactors, Vitamins/Minerals,Hematopoietic Progenitors,Metabolism,Myeloid,Pathways and Processes,Signal Transduction,Stem Cells,Vitamins/Minerals

Customization & Add-ons: Can’t find the antibody you need—or require a custom format for your assay? We can help you source the best match or support custom antibody solutions for diverse research needs, including species and isotype selection, conjugations and labeling (e.g., HRP/AP, biotin, fluorophores), purification grade options (Protein A/G, affinity purified), formulation preferences (buffer selection, carrier-free, glycerol-free), custom concentrations and aliquoting, low-endotoxin options for cell-based work, and application-focused QC/validation support (project dependent). Click Talk to a Scientist to submit a request, email us at support@biohippo.com, or explore our Research Services for additional support—our team will follow up with feasibility details and next steps.