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DNA helicase that acts as an essential component of the spindle assembly checkpoint. De plus, nous expédions Excision Repair Cross-Complementing Rodent Repair Deficiency, Complementation Group 6-Like Anticorps (49) et et beaucoup plus de produits pour cette protéine.
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These findings suggested that ERCC6L, which is highly expressed in breast cancer, acts as an oncogene, is involved in breast cancer development and may serve as a novel molecular target for the treatment of breast cancer.
ERCC6L may stimulates cancer cell proliferation by promoting cell cycle through a way of RAB31-MAPK-CDK2, and it could be a potential biomarker for cancer prognosis and target for cancer treatment.
Data indicate BEND3 as a new interaction partner for PICH in mitosis, and have defined the residues within a TPR-BEN domain interface that mediate this interaction.
Characterization of the NTPR and BD1 interacting domains of the human PICH-BEND3 complex has been reported.
the mitotic roles of PICH and explore further the role of PICH in the timely segregation of the ribosomal DNA locus, are reported.
a novel SUMO-dependent regulation of PICH's function on mitotic centromeres, is reported.
PICH and Topo II cooperate to prevent chromosome missegregation events in mitosis.
PICH is a SUMO-interacting protein and a mitotic SUMO substrate.
PICH recognizes and stabilizes DNA under tension during anaphase, thereby facilitating the resolution of entangled sister chromatids.
PICH protein was required for the correct recruitment to the centromere of active topoisomerase IIalpha, an enzyme specialized in the catenation/decatenation process.
PICH binds to BLM and enables BLM localization to anaphase centromeric threads. PICH and BLM unravel centromeric chromatin and keep anaphase DNA threads mostly free of nucleosomes.
the PICH-Plk1 complex plays a critical role in maintaining prometaphase chromosome architecture
the spindle checkpoint failure formerly attributed to the depletion of PICH most likely reflects an off-target effect that causes the lowering of Mad2 transcript and protein.
These data identify PICH as a novel essential component of checkpoint signaling.
The sensitivity to depletion of topo IIalpha might be linked to structural alterations within the centromere domain, indicated by shortening of the distance across metaphase sister centromeres and persistence of PICH-coated connections.
PICH phosphorylation and its ATPase activity are required for mitotic chromosome compaction through the targeting of Plk1 to chromosome arms.
Functional characterization of the mouse Ercc6l ortholog.
DNA helicase that acts as an essential component of the spindle assembly checkpoint. Contributes to the mitotic checkpoint by recruiting MAD2 to kinetochores and monitoring tension on centromeric chromatin. Acts as a tension sensor that associates with catenated DNA which is stretched under tension until it is resolved during anaphase.
ATP-dependent helicase ERCC6-like
, DNA excision repair protein ERCC-6-like
, Plk1-interacting checkpoint helicase
, SNF2/RAD54 family protein
, excision repair cross-complementing rodent repair deficiency complementation group 6 - like
, excision repair protein ERCC6-like
, tumor antigen BJ-HCC-15
, excision repair cross-complementing rodent repair deficiency complementation group 6-like
, excision repair cross-complementing rodent repair deficiency, complementation group 6-like