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Molecular chaperone (show HSP90AA1 ELISA Kits) SET-assisted eviction of linker histones and Shugoshins is a fundamental step in mammalian mitotic progression.
Aurora B kinase (show AURKB ELISA Kits) interacts with and phosphorylates Sgo1. Aurora B (show AURKB ELISA Kits)-mediated phosphorylation of Sgo1 regulates the distribution of Sgo1 between centromeres and chromosome arms.
SGOL1 variant B induces abnormal mitosis and resistance to taxane in non-small cell lung cancers.
Cohesin complex is shown to be a target of the prophase pathway at centrosomes and protected by Sgo1-dependent PP2A recruitment.
Sgo1 co-recruits Aurora B and PP2A to centromeres of unattached chromosomes.
Data indicate essential role of shugoshin-like protein 1 (Sgo1) in the maintenance of a proper mitotic progression in hepatoma cells and suggest that Sgo1 is a promising oncotarget for hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)).
our findings strongly suggest that CIP2A (show KIAA1524 ELISA Kits) promotes cell cycle progression, premature chromosome segregation, and aneuploidy, possibly through a novel interaction with Sgol1.
Results show that Sgo1 is first recruited to kinetochores by H2A-pT120, and the kinetochore-bound Sgo1 is released by centromeric transcription.
Mutations in SGOL1 cause a novel cohesinopathy affecting heart and gut (show GUSB ELISA Kits) rhythm.
Bub1 (show BUB1 ELISA Kits)-mediated H2A phosphorylation penetrates kinetochores and that this histone mark contributes to a tension-sensitive Sgo1-based molecular switch for chromosome segregation.
Data show that compound mutant spindle assembly checkpoint components BubR1 (show BUB1B ELISA Kits) and Sgo1 embryonic fibroblasts (MEFs) grew at a much slower rate, and a small fraction of cells exhibited morphologies of senescent cells at early passages.
Study established the Sgo1 haploinsufficient mouse as a colon cancer model and identified antagonizing oncogenic and tumor-suppressing pathways that are differentially expressed and may be responsible for the different dynamics in the tumor development.
Sgo1(-/+)-mediated ME-CIN (show PDXP ELISA Kits) strongly promoted/progressed development of hepatocellular carcinoma in the presence of an initiator carcinogen, and it had a mild initiator effect by itself.
Haploinsufficiency of SGO1 results in genomic instability manifested as missegregation of chromosomes and formation of extra centrosomal foci in both murine embryonic fibroblasts and adult bone marrow cells.
It seems that Sgo1 sets up the centromeric protection mechanism in G2, but that its Bub1 (show BUB1 ELISA Kits)-dependent localisation to centromeres during mitosis is not required to maintain cohesion.
Prevention of premature separation of sister chromatids in meiosis I requires the retention of centromeric Sgo1, while normal separation of sister chromatids in meiosis II requires loss of centromeric Sgo1.
report structure and function of the PP2A-shugoshin interaction.
Plays a central role in chromosome cohesion during mitosis by preventing premature dissociation of cohesin complex from centromeres after prophase, when most of cohesin complex dissociates from chromosomes arms. May act by preventing phosphorylation of the stag2 subunit of cohesin complex at the centromere, ensuring cohesin persistence at centromere until cohesin cleavage by espl1/separase at anaphase. May regulate kinetochore microtubule stability in mitosis, possibly to sense tension on mitotic chromosomes.
, shugoshin-like protein
, shugosin centromeric cohesion1
, serologically defined breast cancer antigen NY-BR-85
, shugoshin 1AB protein
, shugoshin 1CD protein
, shugoshin 1EF protein
, shugoshin 1GH protein
, shugoshin 1KL protein
, shugoshin-like 1
, shugoshin 1A protein