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Direct binding of CEP85 to STIL ensures robust PLK4 activation and efficient centriole assembly.
Results from a study on gene expression variability markers in early-stage human embryos shows that STIL is a putative expression variability marker for the 3-day, 8-cell embryo stage.
we observed that depletion of STIL enhanced canonical homologous recombination repair and increased BRCA1 and RAD51 foci in response to DNA double strand breaks. Thus, inhibition of STIL significantly enhances the efficacy of DNA damaging chemotherapeutic drugs in treatment of ovarian cancer.
These data show that complementary mechanisms, such as mother-daughter centriole proximity and CDK1-CyclinB interaction with centriolar components, ensure that centriole biogenesis occurs once and only once per cell cycle, raising parallels to the cell-cycle regulation of DNA replication and centromere formation.
RTTN directly interacts with STIL and acts downstream of STIL-mediated centriole assembly, contributing to building full-length centrioles.
Deletions of Stil is associated with acute T-lymphoblastic leukemia.
Studies indicate that depletion of any one of the protein kinase polo-like kinase 4 (PLK4) and the two proteins STIL and SAS-6 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 and SIL/TAL but a higher incidence of NKX2-5 expression than recorded in Western countries
data provide evidence for novel functions of the human oncogene Stil in neural toxic susceptibility.
The authors suggest that the STIL-coiled-coil region/PLK4 interaction mediates PLK4 activation as well as stabilization of centriolar PLK4 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 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-STIL interaction constitutes a conserved key step in centriole biogenesis
STIL mutation causes autosomal recessive microcephalic lobar holoprosencephaly.
propose that centriole amplification triggered by STIL stabilization is the underlying cause of microcephaly in human patients with corresponding STIL mutations
results provide direct evidence for the involvement of Stil in dopaminergic cell proliferation
A novel function for Stil protein is neural progenitor cell proliferation but not neural differentiation.
Identification of a novel STIL mutation in a family with primary microcephaly.
STIL cooperates with SAS-6 and PLK4 in the control of centriole number and represents a key centriole duplication factor in human cells.
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 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/Lmo2 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