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XEco2 is responsible for Smc3 acetylation and sister chromatid cohesion.
esco2 is upregulated during fin regeneration. esco2 knockdown adversely affects tissue and bone growth in regenerating fins-consistent with role in skeletal morphogenesis. knockdown diminishes cx43 expression which is required for cell-cell communication
This study reveals the dramatic rescue effects of L-leucine stimulation of mTORC1 in RBS cells and supports that normal gene expression and translation requires ESCO2 function.
although many cells required Esco2 to establish cohesion, 10-20% of cells had only weakened cohesion in the absence of Esco2, suggesting that compensatory cohesion mechanisms exist in these cells that undergo a normal mitotic division.
Esco2 depleted zebrafish embryos exhibit features that resemble Roberts Syndrome, including mitotic defects, craniofacial abnormalities and limb truncations.
ESCO2 knockdown inhibits cell proliferation and induces apoptosis in gastric cancer cells.
the involvement of Esco2 in spindle assembly checkpoint and kinetochore functions is mediated by its binding to histone H4 and acetylation of H4K16 both in vivo and in vitro
To Roberts syndrome(RBS), mouse Esco2 turns out to be a cell viability factor, the absence of which results in severe chromosome segregation defects and apoptosis.
ESCO2 may play a vital role in meiosis in both males and females.
Esco2 is needed for cohesin acetylation in PCH and that this modification is required for the proper distribution of cohesin on mitotic chromosomes and for centromeric cohesion
Esco2 promotes neuronal differentiation by repressing Notch signaling.
The analysis of ESCO2 mutants defective in MCM binding indicates that these interactions are required for proper recruitment of ESCO2 to chromatin, cohesin acetylation during DNA replication, and centromeric cohesion.
Several lines of evidence show selective interaction of CRL4s with ESCO2 through LxG motif.
Data indicate that Esco1 and Esco2 contribute to distinct and separable activities of cohesin in vertebrate cells.
ESCO2 knockdown inhibits cell proliferation and induces apoptosis in human gastric cancer cells.
The Esco2 is required for double-strand break (DSB) repair, which is consistent with previous studies in Roberts syndrome(RBS) cells.
the ESCO2 gene mutation responsible for developmental abnormalities maps to chromosome 8p21.
These results demonstrated that the Staf binding site functioned as the basal transcriptional activator of the S phase-specific gene ESCO2, but other mechanisms are required for cell cycle-dependent expression.
In situ hybridisation on human embryos showed ESCO2 expression in the brain, face, limb, kidney and gonads, which corresponds to the structures affected in Roberts syndrome.
ESCO2 has an S-phase specific role in the maintenance of genome stability
required for the establishment of sister chromatid cohesion during S phase
EFO1 and EFO2 are targeted to different chromosome structures to help establish or maintain sister-chromatid cohesion
Inactivating mutations in ESCO2 cause SC phocomelia and Roberts syndrome: there is no phenotype-genotype correlation.
We used Western blot analysis to demonstrate the absence of the ESCO2-truncated protein in cells derived from both fetuses and in a lymphoblastoid cell line derived from the parents.
detection of an ESCO2 frameshift mutation in Roberts syndrome in a Pakistani family
Loss of ESCO2 acetyltransferase activity contributes to the pathogenesis of Roberts syndrome/SC phocomelia.
These results suggest a novel function of Esco2 in transcription repression through modulation of the chromatin structure.
This gene encodes a protein that may have acetyltransferase activity and may be required for the establishment of sister chromatid cohesion during the S phase of mitosis. Mutations in this gene have been associated with Roberts syndrome.
establishment of cohesion 1 homolog 2 (S. cerevisiae)
, N-acetyltransferase ESCO2
, establishment of cohesion 1 homolog 2
, ECO1 homolog 2
, un-named hi2865
, unm hi2865