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Deletions of Stil is associated with acute T-lymphoblastic leukemia.
Studies indicate that depletion of any one of the protein kinase (show CDK7 ELISA Kits) polo-like kinase 4 (PLK4 (show PLK4 ELISA Kits)) and the two proteins STIL and SAS-6 (show SASS6 ELISA Kits) blocks centriole duplication, and, conversely, overexpression causes centriole amplification.
Reconstituting mouse embryonic fibroblasts lacking endogenous Stil, the authors show that STIL oligomerization mediated by these residues is not only important for the centrosomal functions of STIL during the canonical duplication process but also for de-novo formation of centrosomes.
Egyptian T-cell acute lymphoblastic leukemia cases seemed to have a different genetic pattern compared to other populations, with a lower incidence of TLX3/HOX11L2 (show TLX3 ELISA Kits) and SIL (show PMEL ELISA Kits)/TAL (show TALDO1 ELISA Kits) but a higher incidence of NKX2-5 (show NKX2-5 ELISA Kits) expression than recorded in Western countries
data provide evidence for novel functions of the human oncogene (show RAB1A ELISA Kits) Stil in neural toxic susceptibility.
The authors suggest that the STIL-coiled-coil region/PLK4 (show PLK4 ELISA Kits) interaction mediates PLK4 (show PLK4 ELISA Kits) activation as well as stabilization of centriolar PLK4 (show PLK4 ELISA Kits) and plays a key role in centriole duplication.
The STIL p.Gly717Glu mutation was not able to fully restore the centriole duplication failure following depletion of endogenous STIL protein indicating the deleterious role of the mutation.
Negative feedback by centriolar STIL regulates bimodal centriolar distribution of Plk4 (show PLK4 ELISA Kits) and seemingly restricts occurrence of procentriole formation to one site on each parental centriole.
studies provide the first structural insight into how the malfunction of centriole proteins results in human disease and also reveal that the CPAP (show CENPJ ELISA Kits)-STIL interaction constitutes a conserved key step in centriole biogenesis
STIL mutation causes autosomal recessive microcephalic lobar holoprosencephaly.
STIL(-/-) mouse embryos do not contain centrioles or primary cilia, suggesting that these organelles are not essential for mammalian development until mid gestation.
Stil protein regulates centrosome integrity and mitosis through suppression of Chfr.
cloned a mouse homolog of the human SIL promoter
Scl (show TAL1 ELISA Kits) is required for the programming of adult haemangioblasts.
decreased expression of Stil resulted in increased toxic susceptibility of retinal dopaminergic cells to 6-hydroxydopamine
Scl (show TAL1 ELISA Kits)/Lmo2 (show LMO2 ELISA Kits) complex does not appear to autoregulate, as neither gene's expression is affected by depletion of the other
These data, taken together, identify SIL as a novel, vertebrate-specific regulator of mitotic spindle assembly.
This gene encodes a cytoplasmic protein implicated in regulation of the mitotic spindle checkpoint, a regulatory pathway that monitors chromosome segregation during cell division to ensure the proper distribution of chromosomes to daughter cells. The protein is phosphorylated in mitosis and in response to activation of the spindle checkpoint, and disappears when cells transition to G1 phase. It interacts with a mitotic regulator, and its expression is required to efficiently activate the spindle checkpoint. It is proposed to regulate Cdc2 kinase activity during spindle checkpoint arrest. Chromosomal deletions that fuse this gene and the adjacent locus commonly occur in T cell leukemias, and are thought to arise through illegitimate V-(D)-J recombination events. Multiple transcript variants encoding different isoforms have been found for this gene.
Tal1 interrupting locus
, SCL-interrupting locus protein
, TAL-1-interrupting locus protein
, SCL-interrupting locus protein homolog
, TAL1 (SCL) interrupting locus like