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we observed that depletion of STIL enhanced canonical homologous recombination repair and increased BRCA1 and RAD51 (zeige RAD51 Antikörper) 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 (zeige CDK1 Antikörper)-CyclinB (zeige CCNB1 Antikörper) 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 (zeige RTTN Antikörper) 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 (zeige CDK7 Antikörper) polo-like kinase 4 (PLK4 (zeige PLK4 Antikörper)) and the two proteins STIL and SAS-6 (zeige SASS6 Antikörper) 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 (zeige TLX3 Antikörper) and SIL (zeige PMEL Antikörper)/TAL (zeige TALDO1 Antikörper) but a higher incidence of NKX2-5 (zeige NKX2-5 Antikörper) expression than recorded in Western countries
data provide evidence for novel functions of the human oncogene (zeige RAB1A Antikörper) Stil in neural toxic susceptibility.
The authors suggest that the STIL-coiled-coil region/PLK4 (zeige PLK4 Antikörper) interaction mediates PLK4 (zeige PLK4 Antikörper) activation as well as stabilization of centriolar PLK4 (zeige PLK4 Antikörper) 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.
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 (zeige TAL1 Antikörper) 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 (zeige TAL1 Antikörper)/Lmo2 (zeige LMO2 Antikörper) 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