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CDKL5 is a member of Ser/Thr protein kinase family and encodes a phosphorylated protein with protein kinase activity. Additionally we are shipping CDKL5 Proteins (4) and many more products for this protein.
Showing 10 out of 75 products:
Human Polyclonal CDKL5 Primary Antibody for WB - ABIN611314
Barbara, Wrana, Letarte: Endoglin is an accessory protein that interacts with the signaling receptor complex of multiple members of the transforming growth factor-beta superfamily. in The Journal of biological chemistry 1999
Show all 4 references for ABIN611314
Human Polyclonal CDKL5 Primary Antibody for EIA, IHC (p) - ABIN359452
Kalscheuer, Tao, Donnelly, Hollway, Schwinger, Kübart, Menzel, Hoeltzenbein, Tommerup, Eyre, Harbord, Haan, Sutherland, Ropers, Gécz: Disruption of the serine/threonine kinase 9 gene causes severe X-linked infantile spasms and mental retardation. in American journal of human genetics 2003
Show all 2 references for ABIN359452
Human Polyclonal CDKL5 Primary Antibody for IHC (p), WB - ABIN391362
Montini, Andolfi, Caruso, Buchner, Walpole, Mariani, Consalez, Trump, Ballabio, Franco: Identification and characterization of a novel serine-threonine kinase gene from the Xp22 region. in Genomics 1998
Mutations in exon 8 of cyclin-dependent kinase-like 5 gene (show GPD1 Antibodies) were determined to be disease-causing in epileptic encephalopathy.
study presents the genotype of 2 sisters, a CDKL5 mutation c. 283-3_290del, but different phenotype
Data suggest that the increased dosage of cyclin dependent kinase like 5 protein(CDKL5) might have affected interactions of this kinase with its substrates, leading to perturbation of neurodevelopmental and neurobehavioral abnormalities.
It was indicated that CDKL5 controls excitatory synaptic transmission and the conditions associated with CDKL5 deviation in man indicates synaptic abnormalities.
CDKL5 gene mutations accounted for 5.4% of boys with early onset epileptic encephalopathy
CDKL5 gene is not useful in practical molecular diagnosis of atypical Rett syndrome.
Mutations in the CDKL5 gene associtaed with Hanefield variants of Rett syndrome and early-onset epileptic encephalopathies.
study described the clinical condition and characterization of two first Brazilian patients with CDKL5 mutations, including the first Brazilian case of atypical Rett related to abnormalities in this gene
CDKL5 mutations cause severe epilepsy in infancy with subsequent epileptic encephalopathy.
aberrations of CDKL5 and ARX combined are an important consideration in the genetic forms of early-onset epilepsy in boys
these results point to a role of CDKL5 in the early steps of neuronal differentiation that can be explained, at least in part, by its association with shootin1.
Findings highlight a critical role of CDKL5 in the fundamental processes of brain development, namely neuronal precursor proliferation, survival and maturation
Amph1 (show AMPH Antibodies) is the cytoplasmic substrate for CDKL5.
CDKL5 regulates signal transduction pathways and mediates autistic-like phenotypes.
a functional axis between MYCN (show MYCN Antibodies) and CDKL5 governing both neuron proliferation rate and differentiation.
CDKL5 is localized at excitatory synapses and contributes to correct dendritic spine structure and synapse activity.
both subcellular localization and expression of CDKL5 are modulated by the activation of extrasynaptic N-methyl-D-aspartate receptors and suggest regulation of CDKL5 by cell death pathways.
CDKL5 is involved in pre-mRNA processing (show PRPF39 Antibodies), by controlling splicing factor (show SLU7 Antibodies) dynamics.
CDKL5 phosphorylation is required for its entrance into the nucleus whereas a portion of the COOH-terminal domain is responsible for a stable residency in this cellular compartment probably through protein-protein interactions
CDKL5 expression is modulated during neuronal development and its subcellular distribution is tightly regulated by the C-terminal tail
This gene is a member of Ser/Thr protein kinase family and encodes a phosphorylated protein with protein kinase activity. Mutations in this gene have been associated with X-linked infantile spasm syndrome (ISSX), also known as X-linked West syndrome, and Rett syndrome (RTT). Alternate transcriptional splice variants have been characterized.
cyclin-dependent kinase-like 5
, cyclin-dependent kinase-like 5-like
, cyclin dependent kinase 5 transcript
, serine/threonine kinase 9
, serine/threonine-protein kinase 9