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anti-Human CDKL5 Antikörper:
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Human Polyclonal CDKL5 Primary Antibody für 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
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Human Polyclonal CDKL5 Primary Antibody für ICC, IF - ABIN4297085
Ricciardi, Ungaro, Hambrock, Rademacher, Stefanelli, Brambilla, Sessa, Magagnotti, Bachi, Giarda, Verpelli, Kilstrup-Nielsen, Sala, Kalscheuer, Broccoli: CDKL5 ensures excitatory synapse stability by reinforcing NGL-1-PSD95 interaction in the postsynaptic compartment and is impaired in patient iPSC-derived neurons. in Nature cell biology 2012
mutations in the CDKL5 gene in complex genotypes associated with West syndrome with variable phenotype
The genetic etiology of Rett syndrome (RTT) without MECP2, CDKL5, and FOXG1 (zeige FOXG1 Antikörper) mutations is heterogeneous, overlaps with other NDDs, and complicated by a high mutation burden. Dysregulation of chromatin structure and abnormal excitatory synaptic signaling may form two common pathological bases of RTT.
Although abilities were markedly impaired for the majority with the CDKL5 disorder, some females and a few males had better functional abilities. This variability may be related to underlying gene variants, with females with a late truncating variant having better levels of ability than those with no functional protein.
We have characterised the predominant brain isoform of CDKL5, a 9.7 kb transcript comprised of 18 exons with a large 6.6 kb 3'-untranslated region (UTR (zeige UTS2R Antikörper)), which we name hCDKL5_1. In addition we describe new exonic regions and a range of novel splice and UTR (zeige UTS2R Antikörper) isoforms
In the asymptomatic mother, the mutated copy of the CDKL5 gene was inactivated in 90% of blood cells. We also identified a premature stop codon (p.Arg926*) in IQSEC2 (zeige IQSEC2 Antikörper) in a patient with a Rett-like phenotype. Finally, exome sequencing enabled us to characterize a heterozygous de novo missense (p.Val408Ala) in KCNA2 (zeige KCNA2 Antikörper) in a girl with infantile-onset seizures variant of Rett syndrome (RTT)
The results suggested the mutant CDKL5 was responsible for the Rett syndrome disease.
Rett syndrome with early epilepsy and the congenital variant are mainly due to variations in the CDKL5 and FOXG1 (zeige FOXG1 Antikörper) genes, respectively
Mutations in exon 8 of cyclin-dependent kinase-like 5 gene (zeige GPD1 Antikörper) 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.
CDKL5 plays significant roles in regulating emotional behaviors especially on anxiety- and fear-related responses
Study generated the Cdkl5 KO mice, and identified hyperexcitability in response to NMDA and postsynaptic overaccumulation of GluN2B (zeige GRIN2B Antikörper)-containing NMDARs in the hippocampus. The GluN2B (zeige GRIN2B Antikörper)-selective antagonist ifenprodil abrogated the NMDA-induced hyperexcitability of Cdkl5 KO mice. These data indicate that CDKL5 plays an important role in controlling postsynaptic localization of the GluN2B (zeige GRIN2B Antikörper)-SAP102 (zeige DLG3 Antikörper) complex in the hippocampus.
Findings support that CDKL5 plays a role in the comorbid features of autism and ADHD, and mice lacking CDKL5 may serve as an animal model to study the molecular and circuit mechanisms underlying autism-ADHD comorbidity.
data demonstrate that sleep apneas are a core feature of CDKL5 disorder and a respiratory biomarker of CDKL5 deficiency in mice, and suggest that sleep-disordered breathing should be evaluated routinely in CDKL5 patients
The data of this study demonstrate that dendritic spine stabilization is strongly regulated by CDKL5.
Our findings demonstrate that CDKL5 is an important regulator of synaptic function in glutamatergic neurons and serves a critical role in learning and memory.
Nuclear HDAC4 (zeige HDAC5 Antikörper) binds to chromatin as well as to MEF2A (zeige MEF2A Antikörper) transcription factor, leading to histone deacetylation and altered neuronal gene expression. By using a Cdkl5 knockout (Cdkl5 -/Y) mouse model, we found that hypophosphorylated HDAC4 (zeige HDAC5 Antikörper) translocates to the nucleus of neural precursor cells, thereby reducing histone 3 acetylation.
Taken together, these results strongly suggested that DYRK1A (zeige DYRK1A Antikörper) bound to CDKL5 and phosphorylated it on Ser (zeige SIGLEC1 Antikörper)-308, thus interfering with its nuclear localization.
CDKL5 deletion during development more markedly impairs the establishment of a correct GABAergic cerebellar network than that of glutamatergic one, leading to the behavioural symptoms associated with CDKL5 mutation.
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