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CIT encodes a serine/threonine-protein kinase that functions in cell division. Zusätzlich bieten wir Ihnen CIT Antikörper (47) und viele weitere Produktgruppen zu diesem Protein an.
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in this study we have provided evidence that ASPM controls spindle orientation by regulating the dynamics of astral MT and that CITK is a critical downstream partner of ASPM for this activity.
The CIT-K may promote this event by interacting with TUBB3 and by recruiting at the midbody casein kinase-2alpha (CK2alpha) that has previously been reported to phosphorylate the S444 residue.
Data propose that the CC-domain-mediated translocation and actions of Citron-K ensure proper stabilization of the midbody structure during the transition from constriction to abscission.
p27 (zeige CDKN1B Proteine) has a role in cytokinesis via the regulation of citron-K activity
CITRON has a role in proliferation of hepatocellular carcinoma cells
Data report that Discs large (zeige DLG4 Proteine) 5 (Dlg5 (zeige DLG5 Proteine)), a member of the MAGUK family, is an interactor of CitK required for CitK polarization.
Citron-K has a distinct cell cycle-dependent expression pattern and cellular localization as a downstream target of Rho-GTPase (zeige RACGAP1 Proteine) and functions in the control of G(2)/M transition in the hepatocyte cell cycle
Quantitative analysis of citron kinase in cerebral cortex of knockout mice demonstrates that this molecule is involved in differentially regulating the morphology of the dendritic compartment in corticocollicular projecting pyramidal neurons.
These results suggest that the TTC3-RhoA (zeige RHOA Proteine)-CIT-K pathway could be a crucial determinant of in vivo neuronal development, whose hyperactivity may result in detrimental effects on the normal differentiation program.
Lack of citron kinase gene in newborn mice profoundly alters barrelfield cortex cell morphology and number.
Control of abscission requires Eph (zeige EPHA1 Proteine) kinase activity, and Src (zeige SRC Proteine) and citron kinase (CitK) are downstream effectors in the Eph (zeige EPHA1 Proteine)-induced signal transduction cascade
The striking phenotypic overlap between CIT-mutated individuals and the knockout mice and rats that are specifically deficient in the kinase domain supports the proposed causal link between CIT mutation and primary microcephaly in humans.
Splice site variant in CIT, identified in this study, is predicted to abolish splice donor site. cDNA sequence of an affected individual showed retention of an intron next to the splice donor site. The study, presented here, revealed the first variant in the CIT causing Autosomal recessive primary microcephaly in the family.
Biallelic Mutations in Citron Kinase Link Mitotic Cytokinesis to Human Primary Microcephaly
identification of recessively inherited pathogenic variants in CIT as the genetic basis of severe microcephaly and neonatal death; and postmortem data showing that CIT is critical to building a normally sized human brain
Proper midbody architecture requires cross-regulation between two cell division kinases, Citron kinase (CIT-K) and Aurora B (zeige AURKB Proteine), the kinase component of the chromosomal passenger complex.
The TPC1 was shown to interact with citron kinase, with TPC1 overexpression affecting RhoA activity and myosin light chain phosphorylation levels in cytokinesis.
This gene encodes a serine/threonine-protein kinase that functions in cell division. Together with the kinesin KIF14, this protein localizes to the central spindle and midbody, and functions to promote efficient cytokinesis. This protein is involved in central nervous system development. Polymorphisms in this gene are associated with bipolar disorder and risk for schizophrenia. Alternative splicing results in multiple transcript variants.
citron Rho-interacting kinase
, citron kinase
, citron-K kinase
, postsynaptic density protein (citron)
, citron (rho-interacting, serine/threonine kinase 21)
, rho-interacting, serine/threonine-protein kinase 21
, serine/threonine-protein kinase 21