about
DNA damage response pathways in tumor suppression and cancer treatmentProfilin 1 obtained by proteomic analysis in all-trans retinoic acid-treated hepatocarcinoma cell lines is involved in inhibition of cell proliferation and migration.Comparative glycoproteomics based on lectins affinity capture of N-linked glycoproteins from human Chang liver cells and MHCC97-H cells.BRIT1/MCPH1 is essential for mitotic and meiotic recombination DNA repair and maintaining genomic stability in mice.Identification of MYST3 as a novel epigenetic activator of ERα frequently amplified in breast cancer.siRNA-based targeting of cyclin E overexpression inhibits breast cancer cell growth and suppresses tumor development in breast cancer mouse model.Increase in beta1-6 GlcNAc branching caused by N-acetylglucosaminyltransferase V directs integrin beta1 stability in human hepatocellular carcinoma cell line SMMC-7721.Down-regulation of PTEN expression due to loss of promoter activity in human hepatocellular carcinoma cell linesMcph1/Brit1 deficiency promotes genomic instability and tumor formation in a mouse modelS-phase delay in human hepatocellular carcinoma cells induced by overexpression of integrin beta1Role of cell adhesion signal molecules in hepatocellular carcinoma cell apoptosis.mTOR Inhibitors Suppress Homologous Recombination Repair and Synergize with PARP Inhibitors via Regulating SUV39H1 in BRCA-Proficient Triple-Negative Breast Cancer.BRIT1 regulates p53 stability and functions as a tumor suppressor in breast cancer.Comprehensive functional analysis of the tousled-like kinase 2 frequently amplified in aggressive luminal breast cancers.Cadherins Associate with Distinct Stem Cell-Related Transcription Factors to Coordinate the Maintenance of Stemness in Triple-Negative Breast Cancer.Multiple roles of BRIT1/MCPH1 in DNA damage response, DNA repair, and cancer suppression.Microcephalin/MCPH1 associates with the Condensin II complex to function in homologous recombination repair.N-glycosylation affects the adhesive function of E-Cadherin through modifying the composition of adherens junctions (AJs) in human breast carcinoma cell line MDA-MB-435.Overexpression of integrin beta1 inhibits proliferation of hepatocellular carcinoma cell SMMC-7721 through preventing Skp2-dependent degradation of p27 via PI3K pathway.Increased expression of integrin beta1 subunit enhances p21WAF1/Cip1 transcription through the Sp1 sites and p300-mediated histone acetylation in human hepatocellular carcinoma cells.Positive expression of E-cadherin suppresses cell adhesion to fibronectin via reduction of alpha5beta1 integrin in human breast carcinoma cells.Protein phosphatase activity of PTEN inhibited the invasion of glioma cells with epidermal growth factor receptor mutation type III expression.Integrin beta1 subunit overexpressed in the SMMC-7721 cells regulates the promoter activity of p21(CIP1) and enhances its transcription.PKB phosphorylation and survivin expression are cooperatively regulated by disruption of microfilament cytoskeleton.BRCT-domain protein BRIT1 influences class switch recombination.Phosphatidylinositol 3-kinase/protein kinase B pathway stabilizes DNA methyltransferase I protein and maintains DNA methylation.
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description
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Yulong Liang
@ast
Yulong Liang
@en
Yulong Liang
@es
Yulong Liang
@nl
Yulong Liang
@sl
type
label
Yulong Liang
@ast
Yulong Liang
@en
Yulong Liang
@es
Yulong Liang
@nl
Yulong Liang
@sl
prefLabel
Yulong Liang
@ast
Yulong Liang
@en
Yulong Liang
@es
Yulong Liang
@nl
Yulong Liang
@sl
P106
P31
P496
0000-0001-8219-9575