EB2 pS222 antibody
Por um escritor misterioso
Last updated 20 setembro 2024
EB2 S222 site is a target for phosphorylation by the CDKL5 protein kinase; loss-of-function mutations in the human CDKL5 gene are associated with CDKL5 Deficiency Disorder, a neurodevelopmental disorder with intractable epilepsy (Baltussen, Negraes, et al
EB2 pS222 antibody
Chemical genetic identification of CDKL5 substrates reveals its role in neuronal microtubule dynamics. - Abstract - Europe PMC
EB2 pS222 antibody
Epilepsy-linked kinase CDKL5 phosphorylates voltage-gated calcium channel Cav2.3, altering inactivation kinetics and neuronal excitability
JCI - Temporal manipulation of Cdkl5 reveals essential postdevelopmental functions and reversible CDKL5 deficiency disorder–related deficits
PDF) Active human full-length CDKL5 produced in the Antarctic bacterium Pseudoalteromonas haloplanktis TAC125
PDF) Active human full-length CDKL5 produced in the Antarctic bacterium Pseudoalteromonas haloplanktis TAC125
Chemical genetic identification of CDKL5 substrates reveals its role in neuronal microtubule dynamics. - Abstract - Europe PMC
Discovery of a Potent and Selective CDKL5/GSK3 Chemical Probe That Is Neuroprotective
Epilepsy-linked kinase CDKL5 phosphorylates voltage-gated calcium channel Cav2.3, altering inactivation kinetics and neuronal excitability
Discovery and characterization of a specific inhibitor of serine-threonine kinase cyclin-dependent kinase-like 5 (CDKL5) demonstrates role in hippocampal CA1 physiology
Active human full-length CDKL5 produced in the Antarctic bacterium Pseudoalteromonas haloplanktis TAC125, Microbial Cell Factories
Discovery and characterization of a specific inhibitor of serine-threonine kinase cyclin dependent kinase-like 5 (CDKL5) demonstrates role in hippocampal CA1 physiology
Epilepsy-linked kinase CDKL5 phosphorylates voltage-gated calcium channel Cav2.3, altering inactivation kinetics and neuronal excitability
Epilepsy-linked kinase CDKL5 phosphorylates voltage-gated calcium channel Cav2.3, altering inactivation kinetics and neuronal excitability
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