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noncanonical roles of SGO1 drive the clinical manifestations observed in chronic atrial and intestinal dysrhythmia.
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Shugoshin-1 (Sgo1) protects the integrity of the centromeres, and H2A phosphorylation is critical for this process.
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A major function of RSF1 is to recruit HDAC1 to centromeres, where it antagonizes Tip60-mediated acetylation of H2A- K118, which allows Sgo1 accumulation and centromeric cohesion protection.
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Many factors involved in the chromatin association of Shugoshin proteins are well established, most strikingly through modifications found directly on centromeric and pericentric chromatin. It has been well established that phosphorylation at the centromere is essential to nucleating Shugoshin recruitment.
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Molecular chaperone SET-assisted eviction of linker histones and Shugoshins is a fundamental step in mammalian mitotic progression.
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Aurora B kinase interacts with and phosphorylates Sgo1. Aurora B-mediated phosphorylation of Sgo1 regulates the distribution of Sgo1 between centromeres and chromosome arms.
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SGOL1 variant B induces abnormal mitosis and resistance to taxane in non-small cell lung cancers.
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Cohesin complex is shown to be a target of the prophase pathway at centrosomes and protected by Sgo1-dependent PP2A recruitment.
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Sgo1 co-recruits Aurora B and PP2A to centromeres of unattached chromosomes.
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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).
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our findings strongly suggest that CIP2A promotes cell cycle progression, premature chromosome segregation, and aneuploidy, possibly through a novel interaction with Sgol1.
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Results show that Sgo1 is first recruited to kinetochores by H2A-pT120, and the kinetochore-bound Sgo1 is released by centromeric transcription.
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Mutations in SGOL1 cause a novel cohesinopathy affecting heart and gut rhythm.
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Bub1-mediated H2A phosphorylation penetrates kinetochores and that this histone mark contributes to a tension-sensitive Sgo1-based molecular switch for chromosome segregation.
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The most significant association with MaxDrinks was observed with SNP rs11128951 (p = 4.27 x 10(-8)) near SGOL1 gene at 3p24.3.
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Frameshift mutations of SGOL1 and PDS5B and the loss of their expression may be a feature of gastric and colorectal cancers with high microsatellite instability.
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SGO1 promotes multidrug resistance of gastric cancer cells and may be useful as a novel therapeutic target for preventing or reversing multidrug resistance
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Lentivirus-mediated siRNA interference targeting SGO-1 inhibits human NSCLC cell growth
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These results suggest that SGOL1-P1 may function as a negative factor to native SGOL1, and that abundant expression of SGOL1-P1 may be responsible for chromosomal instability.
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HP1alpha binding by INCENP or Shugoshin 1 (Sgo1) is dispensable for centromeric cohesion protection during mitosis of human cells, but might regulate yet unknown interphase functions of the chromosome passenger complex (CPC) or Sgo1 at the centromeres.