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Inhibition of CDK5 in endothelial or hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)) cells reduced HIF-1alpha (show HIF1A ELISA Kits) levels in vitro and in vivo.
One candidate pathway coupling actin filaments to microtubules consists of the actin filament-binding protein drebrin (show DBN1 ELISA Kits) and the microtubule-binding +TIP protein EB3 (show MAPRE3 ELISA Kits). This pathway is regulated proximally by cyclin-dependent kinase 5 phosphorylation of drebrin (show DBN1 ELISA Kits) but the upstream elements in the pathway have yet to be identified.
The CDK5 kinase activates the FAK (show PTK2 ELISA Kits)/AKT (show AKT1 ELISA Kits) signaling pathway to generate VM in a lung cancer cell line, which can help to develop potential therapeutic strategies against vessel-positive tumors.
conditional inactivation of Cdk5 in the jck (show NEK8 ELISA Kits) 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 ELISA Kits) dynamics via its substrate collapsin response mediator protein 2 (show DPYSL2 ELISA Kits).
CRM1 (show XPO1 ELISA Kits) and CDK5 co-expression was an independent prognostic factors for gastric cancer (GC). Combined CRM1 (show XPO1 ELISA Kits) and CDK5 expression could provide a prognostic model for overall survival of GC.
Studies indicate evidence for cyclin dependent kinase 5 (CDK5) in contributing to the onset and progression of tumorigenesis.
this study revealed the functional and mechanistic links between CDK5 and the oncogenic ERK5 (show MAPK7 ELISA Kits)-AP-1 (show FOSB ELISA Kits) signaling pathway in the pathogenesis of colorectal cancer.
the silencing of Cyclin-dependent kinase 5 preventing memory dysfunction
Increased CDK5 expression is associated with breast cancer.
It is shown that p5 binds the kinase at the same CDK5/p25 (show LCN2 ELISA Kits) and CDK5/p35 (show ANXA1 ELISA Kits) interfaces, and is thus a non-selective competitor of both activators, in agreement with available experimental data in vitro.
Cdk5 may play an important role in endoplasmic reticulum stress induced podocyte apoptosis through MEKK1 (show MAP2K1 ELISA Kits)/JNK (show MAPK8 ELISA Kits) pathway in diabetic nephropathy.
Silencing of CDK5 increased BDNF (show BDNF ELISA Kits) expression, temporarily increased phosphorylation of CaMKII (show CAMK2G ELISA Kits), ERK (show EPHB2 ELISA Kits), and CREB (show CREB1 ELISA Kits); and facilitated calcium signaling in neurites. Together, these data suggest that CDK5 downregulation induces synaptic plasticity in mature neurons involving Ca(2 (show CA2 ELISA Kits)+) signaling and BDNF (show BDNF ELISA Kits)/CREB (show CREB1 ELISA Kits) 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 ELISA Kits) can activate several genes that promote neuronal death and aberrant Abeta (show APP ELISA Kits) processing, thereby contributing to the progression of neurodegenerative pathologies.
In this study, we discovered that selective upregulation of p39 (show ATP6V0D1 ELISA Kits) is the underlying mechanism that accommodates the increased functional requirement of Cdk5 activation during neuronal differentiation. In addition, we demonstrated that p39 (show ATP6V0D1 ELISA Kits) 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.
The behavioral and molecular data indicated that TRPV1 (show TRPV1 ELISA Kits) is strongly modulated by Cdk5-mediated phosphorylation at position threonine-407(mouse)/threonine406(rat).
that Cdk5-dependent activation of neuronal inflammasomes was involved in the progression of Parkinson's disease
These data show that Cdk5 regulates the onset and extent of remodeling of the Drosophila mushroom body.
The CDK5 phosphorylates MEKK1 (show MAP3K1 ELISA Kits), and together, they activate the JNK (show MAPK8 ELISA Kits) pathway for apoptosis.
The data of this study demonstrated that Cdk5/p35 (show RPLP0 ELISA Kits) 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 ELISA Kits) cooperate in promoting Cdk5-pY15, which deregulates Cdk5 activity and subcellular localization in Abeta42-triggered neurodegeneration.
Cdk5/p35 (show RPLP0 ELISA Kits) 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 ELISA Kits) and Dpysl3 (show DPYSL3 ELISA Kits) by Cdk5 and DYRK2 (show DYRK2 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) 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