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conditional inactivation of Cdk5 in the jck (zeige 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 (zeige TUBB ELISA Kits) dynamics via its substrate collapsin response mediator protein 2 (zeige DPYSL2 ELISA Kits).
CRM1 (zeige XPO1 ELISA Kits) and CDK5 co-expression was an independent prognostic factors for gastric cancer (GC). Combined CRM1 (zeige 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 (zeige MAPK7 ELISA Kits)-AP-1 (zeige 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 (zeige LCN2 ELISA Kits) and CDK5/p35 (zeige ANXA1 ELISA Kits) interfaces, and is thus a non-selective competitor of both activators, in agreement with available experimental data in vitro.
the activated CDK5 kinase is involved in the EZH2 (zeige EZH2 ELISA Kits) phosphorylation that is required for FBW7 (zeige FBXW7 ELISA Kits)-mediated degradation.
we supposed that EphA4 (zeige EPHA4 ELISA Kits) interacted with CDK5 and promoted its expression which in turn enhanced p-AKT (zeige AKT1 ELISA Kits) expression and promoted cell adhesion-mediated drug resistance in multiple myeloma.
the minor allele of CDK5R1 (zeige CDK5R1 ELISA Kits) 3'-UTR (zeige UTS2R ELISA Kits) rs735555 polymorphism was associated with increased risk for NS-ID. In conclusion, our data suggest that mutations and polymorphisms in CDK5 and CDK5R1 (zeige CDK5R1 ELISA Kits) genes may contribute to the onset of the NS-ID phenotype
Silencing of CDK5 increased BDNF (zeige BDNF ELISA Kits) expression, temporarily increased phosphorylation of CaMKII (zeige CAMK2G ELISA Kits), ERK (zeige EPHB2 ELISA Kits), and CREB (zeige 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 (zeige CA2 ELISA Kits)+) signaling and BDNF (zeige BDNF ELISA Kits)/CREB (zeige 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 (zeige FOXO3 ELISA Kits) can activate several genes that promote neuronal death and aberrant Abeta (zeige APP ELISA Kits) processing, thereby contributing to the progression of neurodegenerative pathologies.
In this study, we discovered that selective upregulation of p39 (zeige 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 (zeige 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 (zeige 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
we demonstrate that Cdk5 phosphorylates collapsin response mediator protein 2 (CRMP2 (zeige DPYSL2 ELISA Kits)) in the dendritic spines of cultured hippocampal neurons and in vivo in the mouse brain. When we eliminated CRMP2 (zeige DPYSL2 ELISA Kits) phosphorylation in CRMP2 (zeige DPYSL2 ELISA Kits)(KI/KI (zeige AXIN1 ELISA Kits)) mice, the densities of dendritic spines significantly decreased in hippocampal CA1 (zeige CA1 ELISA Kits) pyramidal neurons in the mouse brain.
data indicate that PP1alpha (zeige PPP1CA ELISA Kits) is a downstream target of the NGF (zeige NGFB ELISA Kits)/Egr-1 (zeige EGR1 ELISA Kits)/Cdk5 pathway during NGF (zeige NGFB ELISA Kits)-induced differentiation of PC12 cells and suggest that PP1 (zeige PPYR1 ELISA Kits) phosphorylation promotes neuronal differentiation
CDK5-mediated hyperphosphorylation of SIRT1 (zeige 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 (zeige CDK5R1 ELISA Kits) was observed in both cerebral cortex and cerebellum at two months of age
These data show that Cdk5 regulates the onset and extent of remodeling of the Drosophila mushroom body.
The CDK5 phosphorylates MEKK1 (zeige MAP3K1 ELISA Kits), and together, they activate the JNK (zeige MAPK8 ELISA Kits) pathway for apoptosis.
The data of this study demonstrated that Cdk5/p35 (zeige 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 (zeige CDK5R1 ELISA Kits) cooperate in promoting Cdk5-pY15, which deregulates Cdk5 activity and subcellular localization in Abeta42-triggered neurodegeneration.
Cdk5/p35 (zeige 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.
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 (zeige DPYSL2 ELISA Kits) and Dpysl3 (zeige DPYSL3 ELISA Kits) by Cdk5 and DYRK2 (zeige 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.
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