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anti-Human CDK5 Antibodies:
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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 Polyclonal CDK5 Primary Antibody for IP, ELISA - ABIN2472910
Toe: Spinal injuries in Rangoon, Burma. in Paraplegia 1979
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Human Monoclonal CDK5 Primary Antibody for WB - ABIN1945087
Meyerson, Enders, Wu, Su, Gorka, Nelson, Harlow, Tsai: A family of human cdc2-related protein kinases. in The EMBO journal 1992
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Human Monoclonal CDK5 Primary Antibody for WB - ABIN1944859
Li, Liu, Zhang, Ye, Qiao, Ling, Wu, Zhang, Yu: Characterization of a novel human CDK5 splicing variant that inhibits Wnt/beta-catenin signaling. in Molecular biology reports 2010
Show all 2 Pubmed References
Human Polyclonal CDK5 Primary Antibody for IHC, IHC (p) - ABIN4297057
Zhang, Lu, Mao, Ahmed, Yang, Zhou, Jennings, Rodriguez-Aguayo, Lopez-Berestein, Miranda, Qiao, Baladandayuthapani, Li, Sood, Liu, Le, Bast: CDK5 Regulates Paclitaxel Sensitivity in Ovarian Cancer Cells by Modulating AKT Activation, p21Cip1- and p27Kip1-Mediated G1 Cell Cycle Arrest and Apoptosis. in PLoS ONE 2015
Results show that Cdk5 is dysregulated in Alzheimer's disease which suggests an early role in neuronal cell death. Also, Cdk5 activation is under the action of Prx5 via reactive oxygen species-mediated Ca2+-mediated calpain activation.
therapies against ADAM10 (show ADAM10 Antibodies) and ADAM17 (show ADAM17 Antibodies) may promote cancer stem cell migration away from the tumourigenic niche resulting in a differentiated phenotype that is more susceptible to treatment.
axonal impairment in temporal lobe epilepsy may be mediated by NMDAR via GSK-3beta and Cdk5. In addition, inhibiting either NMDARs or GSK-3beta lowered the relative tau phosphorylation level by reversing the decrease of total tau without affecting phosphorylated tau S396 and T231.
Presence of anti-ADAM10 (show ADAM10 Antibodies) auto-Antibodies seems to reflect the increased tumor expression of the immunogenic immature-ADAM10 (show ADAM10 Antibodies) in a group of Colorectal cancer patients, and is associated with a favourable prognosis in patients at stage III of the disease.
ADAM10 (show ADAM10 Antibodies) and ADAM17 (show ADAM17 Antibodies) are the best characterized members of the ADAM (A Disintegrin and Metalloproteinase) - family of transmembrane proteases. Both are involved diverse physiological and pathophysiological processes.For ADAM17 (show ADAM17 Antibodies) phosphatidylserine exposure is required to then induce its shedding function.
A better understanding of the regulatory mechanisms controlling the expression, subcellular localization and activity of ADAM10 (show ADAM10 Antibodies) will likely uncover suitable drug targets which will allow a more specific and fine-tuned modulation of its proteolytic activity
In the present study, the authors show that deletion of a triple serine (3S) motif (Ser (show SIGLEC1 Antibodies)-359 to Ser (show SIGLEC1 Antibodies)-361) adjacent to the cleavage site is sufficient to prevent IL-6R cleavage by ADAM17 (show ADAM17 Antibodies), but not ADAM10 (show ADAM10 Antibodies). We find that the impaired shedding is caused by the reduced distance between the cleavage site and the plasma membrane.
Here, I review some of the proposed functions of ADAM10 (show ADAM10 Antibodies) associated with intestinal crypt homeostasis and tumorigenesis within the gastrointestinal tract in vivo.
In this review, we discuss the contribution of Cdk5 to molecular mechanisms that confer upon tumors the ability to grow, proliferate, and disseminate to secondary organs, as well as resistance to chemotherapies. We subsequently discuss existing and new strategies for targeting Cdk5 and its downstream mechanisms as anticancer treatments.[Review]
Study reports the structure of the ADAM10 (show ADAM10 Antibodies) ectodomain, providing fundamental insights into how substrate selectivity and regulation of catalytic activity is achieved in this important representative of the ADAM family of metalloproteases.
hyperactivation of p25 may temporarily enhance neural progenitor cell proliferation, but impair their long-term survival
Cdk5 directly phosphorylates Cx43 (show GJA1 Antibodies), which regulates the membrane localization and degradation of Cx43 (show GJA1 Antibodies) in neurons.
Cdk5 may play an important role in endoplasmic reticulum stress induced podocyte apoptosis through MEKK1 (show MAP2K1 Antibodies)/JNK (show MAPK8 Antibodies) pathway in diabetic nephropathy.
conditional inactivation of Cdk5 in the jck (show NEK8 Antibodies) 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 (show TUBB Antibodies) dynamics via its substrate collapsin response mediator protein 2 (show DPYSL2 Antibodies).
Silencing of CDK5 increased BDNF (show BDNF Antibodies) expression, temporarily increased phosphorylation of CaMKII (show CAMK2G Antibodies), ERK (show EPHB2 Antibodies), and CREB (show CREB1 Antibodies); and facilitated calcium signaling in neurites. Together, these data suggest that CDK5 downregulation induces synaptic plasticity in mature neurons involving Ca(2 (show CA2 Antibodies)+) signaling and BDNF (show BDNF Antibodies)/CREB (show CREB1 Antibodies) activation.
we report a key role for Cdk5 activity in the development of allogeneic T-cell responses after allogeneic hematopoietic cell transplantation
Cdk5 regulates axon outgrowth through the GRAB-mediated Rab8-Rab11 cascade.
these results show that Cdk5-mediated phospho-regulation of Foxo3 (show FOXO3 Antibodies) can activate several genes that promote neuronal death and aberrant Abeta (show APP Antibodies) processing, thereby contributing to the progression of neurodegenerative pathologies.
In this study, we discovered that selective upregulation of p39 (show ATP6V0D1 Antibodies) is the underlying mechanism that accommodates the increased functional requirement of Cdk5 activation during neuronal differentiation. In addition, we demonstrated that p39 (show ATP6V0D1 Antibodies) selectively directs Cdk5 to phosphorylate protein substrates essential for axonal development, dendritic spine formation, and synaptogenesis. Moreover, our studies suggest opposing roles o
It suggests that ectopic increase of Cdk5 kinase activity through conversion of p35 to p25 is involved in the process of neuronal death induced by hypoxia.
These data show that Cdk5 regulates the onset and extent of remodeling of the Drosophila mushroom body.
The CDK5 phosphorylates MEKK1 (show MAP3K1 Antibodies), and together, they activate the JNK (show MAPK8 Antibodies) pathway for apoptosis.
The data of this study demonstrated that Cdk5/p35 (show RPLP0 Antibodies) 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 (show CDK5R1 Antibodies) cooperate in promoting Cdk5-pY15, which deregulates Cdk5 activity and subcellular localization in Abeta42-triggered neurodegeneration.
Cdk5/p35 (show RPLP0 Antibodies) 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 (show DPYSL2 Antibodies) and Dpysl3 (show DPYSL3 Antibodies) by Cdk5 and DYRK2 (show DYRK2 Antibodies) 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 (show SIRT1 Antibodies) 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 (show CDK5R1 Antibodies) 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.
, a disintegrin and metalloprotease domain 10
, a disintegrin and metalloproteinase domain 10
, disintegrin and metalloproteinase domain-containing protein 10
, kuzbanian protein homolog
, mammalian disintegrin-metalloprotease
, 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