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anti-Human CDK5 Antibodies:
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Human Polyclonal CDK5 Primary Antibody for WB - ABIN540550
Smith, Greer, Tsai: Cdk5 on the brain. in Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 2001
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Human Monoclonal CDK5 Primary Antibody for IP, ELISA - ABIN532627
Shelton, Johnson: Cyclin-dependent kinase-5 in neurodegeneration. in Journal of neurochemistry 2004
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Human Monoclonal CDK5 Primary Antibody for IP, ELISA - ABIN532628
Cruz, Tsai: A Jekyll and Hyde kinase: roles for Cdk5 in brain development and disease. in Current opinion in neurobiology 2004
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Human Polyclonal CDK5 Primary Antibody for IF (p), IHC (p) - ABIN670101
Yin, Qi, Ren, Wang, Jiang, Feng, Cui: Roscovitine treatment caused impairment of fertilizing ability in mice. in Toxicology letters 2015
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Human Monoclonal CDK5 Primary Antibody for FACS, IF - ABIN965844
Choi, Lee, Park, Sung, Lee, Shin, Ryu, Kim: Single-nucleotide polymorphisms in the promoter of the CDK5 gene and lung cancer risk in a Korean population. in Journal of human genetics 2009
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Human Monoclonal CDK5 Primary Antibody for ICC, FACS - ABIN969041
Zhang, Herrup: Cdk5 and the non-catalytic arrest of the neuronal cell cycle. in Cell cycle (Georgetown, Tex.) 2008
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Human Monoclonal CDK5 Primary Antibody for IHC (fro), WB - ABIN5551096
Amin, Zheng, Bk, Shukla, Skuntz, Grant, Steiner, Bhaskar, Pant: The interaction of Munc 18 (p67) with the p10 domain of p35 protects in vivo Cdk5/p35 activity from inhibition by TFP5, a peptide derived from p35. in Molecular biology of the cell 2017
Human Polyclonal CDK5 Primary Antibody for WB - ABIN3042679
Li, Zhang, Zhu, Zhang, Lin, Xu, Yang, Hao, Zhang: A new treatment for cognitive disorders related to in utero exposure to alcohol. in Neural regeneration research 2014
CDK5-dependent phosphorylation and nuclear translocation of TRIM59 promotes macroH2A1 ubiquitination and tumorigenicity.
CDK5, a kinase primarily functional in post-mitotic neurons, is active in late mitotic phases in non-neuronal cells and directly phosphorylates PP4R3beta, the PP4 regulatory subunit that recognizes 53BP1. The results establish CDK5 as a regulator of 53BP1 recruitment.
CDK5 was acting as a promising biomarker in ccRCC patients, and co-expression of CDK5 and p21 is an independent prognostic for overall survival. IHC analysis of CDK5 and p21 on cancer tissues after surgery may help to evaluate and predict the outcome of ccRCC patients.
CDK5 is an important factor in promoting cell proliferation, migration, tyrosinase activity, and melanin production in melanoma cells.
pharmaceutical inhibition of CDK5 prevents glioma stem cell self-renewal in vitro and in xenografted tumors, at least partially by suppressing CREB1 activation independently of PKA/cAMP.
Acetylation-mediated regulation of nuclear CDK5 activity plays a critical role in determining neurite length in embryonic neurons.
The data reveal that CDK5 is activated by PTN, in an RPTPbeta-zeta-dependent manner, regulates PTN-induced cell migration and is an attractive target for the inhibition of PTN pro-angiogenic properties.
Cdk5-induced oxidative stress upregulates ALDH1A1 transcription. Cdk5 increases ALDH1A1 levels by preventing its ubiquitylation via direct phosphorylation
CDK5 can regulate the expression of PD-L1, and its presence is critical for the maturation of dendritic cells. CDK5 may play an important role in the pathogenesis of chronic rhinosinusitis with nasal polyps disease
A novel phosphoregulatory site Serine-47 on CDK5.Phosphorylation of S47 on CDK5 presents a quick, physiologically relevant mechanism to help cells conform to the proliferation-migration dichotomy.
Apoptosis in breast cancer cells due to Cdk5 loss occurs via a novel mPTP-dependent mechanism that acts primarily through Reactive oxygen species increase.
CDK5 SNPs are associated with inattention, domain specific impulsivity, behavioral problem, cognitive function and co-morbidity in ADHD.
A decrease in CDK5 and MAPT gene expression was found in Alzheimer's disease (AD) patients' brains, significant differences were found in CDK5 expression in the hippocampus and the entorhinal cortex. In both cases, mRNA was lower in the AD group); however, the same analysis using the MAPT gene revealed no significant statistical differences.
Study discovered a new mechanism of regulation of CDK5 through loss of CDCP1, which dynamically regulates beta1-integrin in non-adherent cells and which may promote vascular dissemination in patients with advanced prostate cancer.
Authors identified and validated cyclin-dependent kinase 5 (CDK5) as the targeting gene of ARNTL by dual Luciferase reporter assay and chromatin immunoprecipitation assay.
Study finds that CDK5, 14-3-3 epsilon, and KIAA0528 are all essential for cytoplasmic dynein force adaptation and that they regulate the transport of lipid droplets, lysosomes, and mitochondria.
Study is the first to report that PP2A may affect metastasis by interacting with CDK5 in gastric cancer (GC) and that low levels of PP2A may indicate a tendency for poor prognosis in patients with GC.
Result show that CDK5 mediates the phosphorylation of XBP1 at residue Ser61.
Our findings demonstrate that TRPA1 is a substrate of Cdk5 and that Cdk5 activity is also able to modulate TRPA1 agonist-induced calcium influx and chemo-nociceptive behavioral responses.
High CDK5 expression is associated with Parkinson's disease.
CDK5 is an important factor in promoting cell proliferation, migration, tyrosinase activity, and melanin production in melanoma cells, with an essential regulatory role for p-CREB.
results show that a Nestin-Cdk5-Drp1 axis negatively regulates mitochondrial OXPHOS, which is indispensable for the maintenance of NSPC stemness.
data indicate that Drp1 is a direct target of Cdk5, and Cdk5-mediated phosphorylation of Drp1 at Serine 579 regulates Abeta1-42 induced mitochondrial fission and neuronal toxicity.
Cdk5 downstream targets involved in memory and learning decline differ depending on the brain region analyzed suggesting that distinct Cdk5 effectors could be involved in cognitive impairments in Huntington's disease.
The novel roles of Cdk5 in oligodendrocyte lineage cells may provide insights for helping understand the cognitive changes sometimes seen in demyelinating diseases such as multiple sclerosis
these results indicate that phosphorylation of CHIP at Ser20 by Cdk5 activation inhibits CHIP-mediated truncated apoptosis-inducing factor (tAIF) degradation, thereby contributing to tAIF-induced neuronal cell death following rotenone treatment
Identification of candidate lncRNAs regulated by Cdk5 in mouse skin.
These results of this study suggest that a physiological role of Cdk5 in visual cortex is to consolidate and stabilize neural circuits through controlling GABAergic signaling.
Mcl-1 is a disease-specific target of Cdk5, which associates with Cdk5 under basal conditions, but is not regulated by it.
Selective loss of Cdk5 in dorsolateral striatum increased locomotor activity and attenuated motor learning.
CDK5-mediated phosphorylation of Sirt2 has a role in to depressive-like behavior induced by social defeat stress
findings collectively demonstrate that the Cdk5-dependent phosphorylation of liprinalpha1 is important for the postsynaptic organization during activity-dependent synapse development.
Study generated Purkinje cell-specific p35; p39 double knockout, L7cre-p35f/f; p39-/- mice and found there were ectopic Purkinje cells scattered singly or in groups over the cerebellar cortex due to Cdk5-loss-dependent migration failure. Selective loss of Cdk5 activity in Purkinje cells contributed to motor impairments. TrkB agonist treatment partially rescued Purkinje cell morphological defects of dendritic structures.
Stress-induced nuclear translocation of CDK5 suppresses neuronal death by downregulating ERK activation via VRK3 phosphorylation
hyperactivation of p25 may temporarily enhance neural progenitor cell proliferation, but impair their long-term survival
Cdk5 directly phosphorylates Cx43, which regulates the membrane localization and degradation of Cx43 in neurons.
Cdk5 may play an important role in endoplasmic reticulum stress induced podocyte apoptosis through MEKK1/JNK pathway in diabetic nephropathy.
conditional inactivation of Cdk5 in the jck mice significantly attenuates cystic disease progression and is associated with shortening of ciliary length as well as restoration of cellular differentiation. Our results suggest that CDK5 may regulate ciliary length by affecting tubulin dynamics via its substrate collapsin response mediator protein 2.
Silencing of CDK5 increased BDNF expression, temporarily increased phosphorylation of CaMKII, ERK, and CREB; and facilitated calcium signaling in neurites. Together, these data suggest that CDK5 downregulation induces synaptic plasticity in mature neurons involving Ca(2+) signaling and BDNF/CREB activation.
we report a key role for Cdk5 activity in the development of allogeneic T-cell responses after allogeneic hematopoietic cell transplantation
This result suggests that attenuating CDK5-mediated phosphorylation of CP190 may enhance its in vivo insulator activity at the gypsy transposon
These data indicate that Cdk5 is required to maintain the protective role of basal autophagy in the initial responses to a subset of neurodegenerative challenges via phosphorylating Acinus at serine 437.
These data show that Cdk5 regulates the onset and extent of remodeling of the Drosophila mushroom body.
The CDK5 phosphorylates MEKK1, and together, they activate the JNK pathway for apoptosis.
The data of this study demonstrated that Cdk5/p35 kinase is a key regulator of the development and maintenance of the axon initial segment in Drosophila.
Therefore, we propose that Abl and p35/p25 cooperate in promoting Cdk5-pY15, which deregulates Cdk5 activity and subcellular localization in Abeta42-triggered neurodegeneration.
Cdk5/p35 did not have major effects on tau toxicity or phosphorylation.
In Drosophila the cdk5 is needed for locomotive behavior and NMJ elaboration.
data indicate that PP1alpha is a downstream target of the NGF/Egr-1/Cdk5 pathway during NGF-induced differentiation of PC12 cells and suggest that PP1 phosphorylation promotes neuronal differentiation
The intrahepatic biliary network is a highly branched three-dimensional network lined by biliary epithelial cells. We designed a new computer-based algorithm that quantitatively computes the structural differences of the three-dimensional networks. Utilizing the algorithm, we showed that inhibition of Cyclin-dependent kinase 5 (Cdk5) led to reduced branching in the intrahepatic biliary network.
These results suggest that the phosphorylation of Dpysl2 and Dpysl3 by Cdk5 and DYRK2 is required for the proper positioning of Rohon-Beard neurons and neural crest cells during neurulation in zebrafish embryos.
cdk5 mRNA was injected into the one- to two-cell embryos, in which neuron apoptosis was inhibited compared with the uninjected control embryos.
we have cloned and characterized the zebrafish cdk5 ortholog. Zebrafish cdk5 is 96% identical to its human counterpart and expressed as early as the blastula stage.
cdk5 plays a critical role in spinal and cranial motor neuron development.
CDK5-mediated hyperphosphorylation of SIRT1 facilitates the development of endothelial senescence and atherosclerosis.
CDK5 mRNA reaches the highest level in cerebral cortex at two months of age and in cerebellum and liver at 4 months of age, respectively, whereas the peak level of CDK5R1 was observed in both cerebral cortex and cerebellum at two months of age
CDK-5 regulates DCV polarity by both promoting DCV trafficking in axons and preventing dynein-dependent DCV trafficking into dendrites.
Cdk-5 facilitates new synapse formation by regulating the transport of synaptic vesicles to the sites of synaptogenesis.
CDK-5 promotes the anterograde trafficking of GLR-1 and that phosphorylation of LIN-10 may play a role in this process.
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, oligodendrocytes differentiation, synaptic plasticity and neurotransmission, by phosphorylating key proteins. Activated by interaction with CDK5R1 (p35) and ATP6V0D1 (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 PCTAIRE 1/CDK16 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 elicites 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.
TPKII catalytic subunit
, cell division protein kinase 5
, protein kinase CDK5 splicing
, serine/threonine-protein kinase PSSALRE
, tau protein kinase II catalytic subunit
, CR6 protein kinase
, proline-directed protein kinase 33 kDa subunit
, neuronal cyclin-dependent kinase 5
, Cell division protein kinase 5
, cyclin-dependent-like kinase 5