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The protein encoded by SALL4 may be a zinc finger transcription factor. Additionally we are shipping SALL4 Antibodies (67) and SALL4 Kits (1) and many more products for this protein.
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These results suggest that Sall4, activated by posteriorizing signals, represses the pou5f3 genes to provide a permissive environment.
SAL family member (XlSALL4) is expressed at the right place and time to play a role regulating both digit identity along the anterior/posterior axis and epimorphic limb regeneration
Sall4 expression expression in chemosensory cells implicates this transcription factor in the development and renewal of taste epithelia in zebrafish.
Sall gene family redundancy and tbx5 (show TBX5 Proteins) offer explanations for the similarity of individuals with Okihiro syndrome and Holt-Oram syndrome limb defects
As SALL4A is known to impair ZBTB16 (show ZBTB16 Proteins)-mediated Kit repression , our study provides novel insights into the molecular mechanism by which ATRA could control KIT expression, and thereby the differentiation of Aal into A1 spermatogonia in vivo.
In differentiated ESCs (show NR2E3 Proteins), Sall4 bound to these somatic cell program gene loci, which are reportedly occupied by Prdm1 (show PRDM1 Proteins) in embryonic carcinoma cells.
This study identified a critical role of the Sall4-Gli3 (show GLI3 Proteins) system at the early steps of limb development for proper development of the appendicular skeletal elements.
Sall4 also interacts with Baf60a (show SMARCD1 Proteins), a member of the SWI (show SMARCA1 Proteins)/SNF (show SNRPA Proteins) (switch/sucrose nonfermentable) ATP-dependent chromatin-remodeling complex, which is responsible for recruiting Sall4 to the site of DNA DSB damage.
SALL4b is the major isoform in hematopoietic stem cell (show BCL11A Proteins)s. Overexpression of either isoform impairs hematopoietic colony formation. Lineage-negative bone marrow overexpressing SALL4b fails to engraft. SALL4a or SALL4b overexpression impairs hematopoiesis.
our data revealed that histone demethylase LSD1 (show KDM1A Proteins) may negatively regulate SALL4-mediated transcription, and the dynamic regulation of SALL4-associated epigenetic factors cooperatively modulates early hematopoietic precursor proliferation.
Oct4, Sall4, and Nanog form a robust and integrated network to govern mammalian pre-implantation development.
these results indicate that 1) SALL4 isoforms are differentially expressed at the initiation of spermatogenesis
Sall4 contributes to the transcriptional network operating in pluripotent cells together with Oct-3/4 (show POU5F1 Proteins) and Sox2 (show SOX2 Proteins)
SALL4 and KLF5 (show KLF5 Proteins) were aberrantly expressed in the CDX1 (show CDX1 Proteins)(+) intestinal metaplasia of the stomach. Sustained expression of CDX1 (show CDX1 Proteins) gave rise to the induction of early intestinal-stemness markers, followed by the expression of intestinal-differentiation markers.
SALL4 was highly expressed and correlated with poor prognosis in SOC (show UBXN11 Proteins) patients, promoting invasion and metastasis of OC cells.
Study reports a novel heterozygous frameshift insertion in SALL4, c.410dupG (p.Gly138Argfs*43) segregating with Okihiro syndrome in a Brazilian pedigree with five affected individuals; the c.410dupG variant in SALL4 gene reported here is the cause of Okihiro syndrome without Duane anomaly, but with foot defect in one affected individual.
By inhibition of SALL4 expression, the proliferation, invasiveness and drug resistance were dramatically reduced while apoptosis rate was up-regulated.
SALL4 expression in squamous cell carcinoma of the esophagus may constitute a sign of dedifferentiation leading to poor patient prognosis
SALL4 has an oncogenic role in intrahepatic cholangiocarcinoma
review aims to summarize our current knowledge of SALL4, including a SALL4-based approach to classify and target cancers
SALL4 could induce Epithelial-mesenchymal transition and resistance to antineoplastic drugs through the regulation of c-Myc (show MYC Proteins). SALL4 and c-Myc (show MYC Proteins) may be novel therapeutic targets for endometrial cancer.
The results show that miR (show MLXIP Proteins)-219-5p inhibited carcinogenesis of colon cancer by targeting oncogene (show RAB1A Proteins) Sall4
An atypical 0.73 MB microduplication of 22q11.21 and a novel SALL4 missense mutation associated with thumb agenesis and radioulnar synostosis.
The mechanism through which miR (show MLXIP Proteins)-33b inhibits the stemness, migration and invasion of breast cancer cells is by targeting HMGA2, SALL4 and Twist1 (show TWIST1 Proteins).
The protein encoded by this gene may be a zinc finger transcription factor. Defects in this gene are a cause of Duane-radial ray syndrome (DRRS).
sal-like 4 (Drosophila)
, sal-like protein 4-like
, sal-like 4
, zinc finger transcription factor SALL4 a
, sal-like protein 4
, zinc finger protein SALL4
, zinc finger protein 797