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Data show that both sall1 (show SALL1 ELISA Kits) 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 ELISA Kits) 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 and SALL4 regulatory targets in undifferentiated spermatogonia.
study explores a pivotal role of Sall4 in regulating epigenetic maturation of mouse oocytes.
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 study showed that SALL4 plays an important role in regulating the proliferation, migration, and invasion of osteosarcoma cells.
The SALL4 - integrin alpha6 - integrin beta1 network promotes cell migration for metastasis via activation of focal adhesion dynamics in basal-like breast cancer cells.
Coexpression of SALL4 with HDAC1 and/or HDAC2 was associated with PTEN underexpression and a poor prognosis in hepatocellular carcinoma.
demethylation of CpGs located within OCT4 (show POU5F1 ELISA Kits) and STAT3 (show STAT3 ELISA Kits) cis (show CISH ELISA Kits)-acting elements, downstream of SALL4 TSS (show RPL38 ELISA Kits), enables OCT4 (show POU5F1 ELISA Kits) and STAT3 (show STAT3 ELISA Kits) binding, recruitment of BRG1 (show SMARCA4 ELISA Kits), and enhanced RNA polymerase II elongation and SALL4 transcription
SALL4 was expressed in 100% of choriocarcinomas and it was not detected in any placental site trophoblastic tumor and epithelioid trophoblastic tumor.
SALL4 is useful for subtyping hepatoblastoma, and high SALL4 expression is associated with decreased survival in hepatoblastoma.
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 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