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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 ELISA Kits) offer explanations for the similarity of individuals with Okihiro syndrome and Holt-Oram syndrome limb defects
JARID2 (show JARID2 ELISA Kits) physically interacts with ESRRB (show ESRRB ELISA Kits), SALL4A, and PRDM14 (show PRDM14 ELISA Kits)
As SALL4A is known to impair ZBTB16-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 ELISA Kits), Sall4 bound to these somatic cell program gene loci, which are reportedly occupied by Prdm1 (show PRDM1 ELISA Kits) in embryonic carcinoma cells.
This study identified a critical role of the Sall4-Gli3 (show GLI3 ELISA Kits) system at the early steps of limb development for proper development of the appendicular skeletal elements.
Sall4 also interacts with Baf60a (show SMARCD1 ELISA Kits), a member of the SWI (show SMARCA1 ELISA Kits)/SNF (show SNRPA ELISA Kits) (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 cells. 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 (show MBD2 ELISA Kits) LSD1 (show KDM1A ELISA Kits) 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 ELISA Kits) and Sox2 (show SOX2 ELISA Kits)
miR33b suppresses the proliferation and metastasis of hepatocellular carcinoma cells through the inhibition of SALL4 expression.
this study demonstrates that miR-16 (show GDE1 ELISA Kits) plays a suppressive role in regulating cell proliferation, migration and invasion, and EMT (show ITK ELISA Kits) in glioma, at least in part by directly targeting SALL4.
We evaluate the effects of siRNA-inhibited expression of the SALL4 gene on the proliferation, colony formation, and apoptosis of prostate cancer C4-2 cells. Silencing SALL4 expression by using siRNA technology inhibited the proliferation and colony formation of C4-2 cells, and promoted apoptosis likely mediated by Bcl-2 (show BCL2 ELISA Kits) and Bax (show BAX ELISA Kits) expression.
the under-expression of SOX1 (show SOX1 ELISA Kits) was associated significantly with SALL4 overexpression. This study was the first to evaluate SOX1 (show SOX1 ELISA Kits) underexpression and its association with poor prognosis in esophageal squamous cell carcinoma.
Hepatocellular carcinoma patients with higher expression levels of SALL4 and AFP (show AFP ELISA Kits) have worse prognosis.
Persistent expression of SALL4 in metastatic MGCTs resistant to chemoradiation also raises the possibility for targeted systemic therapy as the anti-SALL4 peptide continues to be developed
SALL4 and beta-catenin (show CTNNB1 ELISA Kits) were positively correlated in colorectal cancer.
SALL4 was highly expressed and correlated with poor prognosis in SOC (show UBXN11 ELISA Kits) 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.
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