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anti-Human CDK5 Antikörper:
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Human Polyclonal CDK5 Primary Antibody für 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 für 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 für 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 für WB - ABIN1944859
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 für WB - ABIN1945087
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
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Human Polyclonal CDK5 Primary Antibody für IP, ELISA - ABIN2472910
Toe: Spinal injuries in Rangoon, Burma. in Paraplegia 1979
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Human Polyclonal CDK5 Primary Antibody für 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
Presence of anti-ADAM10 (zeige ADAM10 Antikörper) auto-Antibodies seems to reflect the increased tumor expression of the immunogenic immature-ADAM10 (zeige ADAM10 Antikörper) in a group of Colorectal cancer patients, and is associated with a favourable prognosis in patients at stage III of the disease.
ADAM10 (zeige ADAM10 Antikörper) and ADAM17 (zeige ADAM17 Antikörper) 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 (zeige ADAM17 Antikörper) 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 (zeige ADAM10 Antikörper) 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 (zeige SIGLEC1 Antikörper)-359 to Ser (zeige SIGLEC1 Antikörper)-361) adjacent to the cleavage site is sufficient to prevent IL-6R cleavage by ADAM17 (zeige ADAM17 Antikörper), but not ADAM10 (zeige ADAM10 Antikörper). 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 (zeige ADAM10 Antikörper) 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 (zeige ADAM10 Antikörper) 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.
Data suggest that ADAM10 (zeige ADAM10 Antikörper) associates directly with all members of a subgroup of tetraspanins having eight cysteines in the large extracellular domain ('TspanC8'): Tspan5 (zeige TSPAN5 Antikörper), Tspan10, Tspan14, Tspan15 (zeige TSPAN15 Antikörper), Tspan17, and Tspan33 (zeige TSPAN33 Antikörper). [REVIEW]
Inhibition of CDK5 in endothelial or hepatocellular carcinoma (HCC (zeige FAM126A Antikörper)) cells reduced HIF-1alpha (zeige HIF1A Antikörper) levels in vitro and in vivo.
Results found ADAM10 (zeige ADAM10 Antikörper) expression under the regulation of MIR (zeige MLXIP Antikörper)-655 which binds the 3'-UTR (zeige UTS2R Antikörper) of ADAM10 (zeige ADAM10 Antikörper) mediating the progression of hepatocellular carcinoma.
hyperactivation of p25 may temporarily enhance neural progenitor cell proliferation, but impair their long-term survival
Cdk5 directly phosphorylates Cx43 (zeige GJA1 Antikörper), which regulates the membrane localization and degradation of Cx43 (zeige GJA1 Antikörper) in neurons.
Cdk5 may play an important role in endoplasmic reticulum stress induced podocyte apoptosis through MEKK1 (zeige MAP2K1 Antikörper)/JNK (zeige MAPK8 Antikörper) pathway in diabetic nephropathy.
conditional inactivation of Cdk5 in the jck (zeige NEK8 Antikörper) 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 Antikörper) dynamics via its substrate collapsin response mediator protein 2 (zeige DPYSL2 Antikörper).
Silencing of CDK5 increased BDNF (zeige BDNF Antikörper) expression, temporarily increased phosphorylation of CaMKII (zeige CAMK2G Antikörper), ERK (zeige EPHB2 Antikörper), and CREB (zeige CREB1 Antikörper); and facilitated calcium signaling in neurites. Together, these data suggest that CDK5 downregulation induces synaptic plasticity in mature neurons involving Ca(2 (zeige CA2 Antikörper)+) signaling and BDNF (zeige BDNF Antikörper)/CREB (zeige CREB1 Antikörper) 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 Antikörper) can activate several genes that promote neuronal death and aberrant Abeta (zeige APP Antikörper) processing, thereby contributing to the progression of neurodegenerative pathologies.
In this study, we discovered that selective upregulation of p39 (zeige ATP6V0D1 Antikörper) is the underlying mechanism that accommodates the increased functional requirement of Cdk5 activation during neuronal differentiation. In addition, we demonstrated that p39 (zeige ATP6V0D1 Antikörper) 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 (zeige MAP3K1 Antikörper), and together, they activate the JNK (zeige MAPK8 Antikörper) pathway for apoptosis.
The data of this study demonstrated that Cdk5/p35 (zeige RPLP0 Antikörper) 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 Antikörper) cooperate in promoting Cdk5-pY15, which deregulates Cdk5 activity and subcellular localization in Abeta42-triggered neurodegeneration.
Cdk5/p35 (zeige RPLP0 Antikörper) 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 (zeige DPYSL2 Antikörper) and Dpysl3 (zeige DPYSL3 Antikörper) by Cdk5 and DYRK2 (zeige DYRK2 Antikörper) 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 (zeige SIRT1 Antikörper) 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 Antikörper) 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