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Data show that both sall1 and sall4 act to repress pou5f3 (oct4)family gene expression in the neural plate, thereby allowing vertebrate neural development to proceed.
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
Study propose a model whereby enhancer binding by Sall4 and other pluripotency-associated transcription factors is responsible for maintaining the balance between transcriptional programmes in pluripotent cells.
SALL4 has a negative impact in DNA damage repair, and support the model of dual functional properties of SALL4 in leukemogenesis through inhibiting DNA damage repair and promoting cell survival.
these data reveal the full profile of PLZF (show ZBTB16 Proteins) and SALL4 regulatory targets in undifferentiated spermatogonia.
study explores a pivotal role of Sall4 in regulating epigenetic maturation of mouse oocytes.
JARID2 (show JARID2 Proteins) physically interacts with ESRRB, SALL4A, and PRDM14 (show PRDM14 Proteins)
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 cells. Overexpression of either isoform impairs hematopoietic colony formation. Lineage-negative bone marrow overexpressing SALL4b fails to engraft. SALL4a or SALL4b overexpression impairs hematopoiesis.
SALL4 is a target gene of miR (show MLXIP Proteins)-181b in glioma.SALL4 is upregulated in glioma.
SALL4 is a target gene of mir (show MLXIP Proteins)-98 in non-small cell lung cancer cells.
miR (show MLXIP Proteins)-98 plays a suppressive role in the proliferation, migration, invasion and EMT (show ITK Proteins) of HCC (show FAM126A Proteins) cells, partly at least, via directly inhibition of SALL4.
SALL4 immunopositivity is not a prognostic factor in Combined hepatocellular carcinoma (HCC (show FAM126A Proteins)) and cholangiocarcinoma (CC) (cHCC-CC); however, it is associated with alpha-fetoprotein (show AFP Proteins), glypican 3 (show GPC3 Proteins) and EpCAM (show EPCAM Proteins) immunopositivity, indicating the mechanism of carcinogenesis.
these data suggest that Bmi-1 (show BMI1 Proteins) could serve as a novel prognostic biomarker in pediatric primary acute lymphoblastic leukemia (ALL)and may be partially regulated by Sall4a. Our study also showed that Bmi-1 (show BMI1 Proteins) could serve as a new therapeutic target for the treatment of pediatric ALL.
SALL4 overexpression is associated with neoplasms.
Findings indicate that long-term exposure to IM results in dysregulation of stem cell renewal-regulatory Hippo (MST1 (show MST1 Proteins)/2)/YAP (show YAP1 Proteins) signaling, and that inhibition of miR (show MLXIP Proteins)-181a using a microRNA sponge inhibitor resulted in decreased transcription of SOX2 (show SOX2 Proteins) and SALL4.
Study showed that SALL4 was overexpressed in a majority of human esophageal squamous cell carcinoma (ESCC) tissues and that aberrantly activated SALL4 may contribute to esophageal tumorigenesis by promoting malignant proliferation and inhibiting cell apoptosis, regulating esophageal squamous cell migration, invasion and cell cycle.
Data show that SALL4 promotes the expression of Glut1 (show SLC2A1 Proteins) and open chromatin through a HP1alpha (show CBX5 Proteins)-dependent mechanism.
Our report is the first description of structural eye defects associated with two missense variants in SALL4 inherited in trans; the absence of reported findings in both parents suggests that both sequence variants are hypomorphic mutations and that both are needed for the ocular phenotype.
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