sall4造句

• Furthermore, canonical Wnt signaling has been proposed to activate " SALL4 " gene expression in both development and in cancer.
• This interaction is best characterized in the co-regulation of " HOXA9 " gene by SALL4 and MLL in leukemic cells.
• In mouse ESCs, Sall4 was found to bind the essential stem cell factor, octamer-binding transcription factor 4 ( PTEN ).
• SALL4 binds the " PTEN " promoter and recruits the NuRD complex to mediate its repression, thus leads to proliferation of cells.
• POU5F1, TDGF1 ( CRIPTO ), SALL4, LECT1, and BUB1 are also related genes all responsible for self-renewal and pluripotent differentiation.
• In breast cancer, Signal transducer and activator of transcription 3 ( STAT3 ) has been reported to directly activate " SALL4 " expression.
• It is unclear how SALL4 expression is de-regulated in malignant cells, but DNA hypomethylation in its intron 1 region has been observed in B-ALL.
• SALL4 has at least one canonical MLL ) protein, which is a homolog of Drosophila Trithorax and yeast Set1 proteins and has histone 3 lysine 4 ( H3K4 ) trimethylation activity.
• The various SALL4-null mouse models mimic human mutations in the " SALL4 " gene, which were shown to cause developmental problems in patients with HCC, and esophageal squamous cell carcinoma.
• The various SALL4-null mouse models mimic human mutations in the " SALL4 " gene, which were shown to cause developmental problems in patients with HCC, and esophageal squamous cell carcinoma.
• SALL4 contains one zinc finger in its amino ( N-) terminus and three clusters of zinc fingers that each coordinates zinc with two cysteines and two histidines ( Cys 2 His 2-type ) that potentially confer nucleic acid binding activity.
• JDP2, which has been shown to regulate Wnt signaling pathway and prevent ROS production, Moreover, they showed that JDP2 anchors five non-Yamanaka factors ( ID1, LRH1, SALL4, and GLIS1 ) to reprogram mouse embryonic fibroblasts into iPSCs.
• Further elucidating its tumorigenesis function, knocking down " SALL4 " expression with short hairpin-RNA in leukemic cells or treating these cells with a peptide that mimics the N-12aa of SALL4 to inhibit its interaction with the NuRD complex both result in cell death.
• Further elucidating its tumorigenesis function, knocking down " SALL4 " expression with short hairpin-RNA in leukemic cells or treating these cells with a peptide that mimics the N-12aa of SALL4 to inhibit its interaction with the NuRD complex both result in cell death.