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anti-Rat (Rattus) SALL4 Antibodies:
anti-Mouse (Murine) SALL4 Antibodies:
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Human Monoclonal SALL4 Primary Antibody for IHC (p), ELISA - ABIN566099
Cauffman, De Rycke, Sermon, Liebaers, Van de Velde: Markers that define stemness in ESC are unable to identify the totipotent cells in human preimplantation embryos. in Human reproduction (Oxford, England) 2008
Show all 17 Pubmed References
Human Polyclonal SALL4 Primary Antibody for WB - ABIN388303
Yang, Chai, Liu, Fink, Lin, Silberstein, Amin, Ward, Ma: Bmi-1 is a target gene for SALL4 in hematopoietic and leukemic cells. in Proceedings of the National Academy of Sciences of the United States of America 2007
Show all 4 Pubmed References
Human Polyclonal SALL4 Primary Antibody for ELISA, WB - ABIN4369825
Paradisi, Arias: IVIC syndrome is caused by a c.2607delA mutation in the SALL4 locus. in American journal of medical genetics. Part A 2007
Show all 3 Pubmed References
Mouse (Murine) Polyclonal SALL4 Primary Antibody for ELISA, WB - ABIN547920
Wang, Rao, Chu, Shen, Levasseur, Theunissen, Orkin: A protein interaction network for pluripotency of embryonic stem cells. in Nature 2006
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 offer explanations for the similarity of individuals with Okihiro syndrome and Holt-Oram syndrome limb defects
Findings indicate that SALL4 critically contributes to MLL-AF9-induced leukemia, unraveling the underlying transcriptional and epigenetic mechanisms in this disease.
SALL4 associated with the NuRD co-repressor and repressed expression of the tumor suppressor genes Foxl1 and Dusp4.
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 physically interacts with ESRRB, SALL4A, and PRDM14
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, Sall4 bound to these somatic cell program gene loci, which are reportedly occupied by Prdm1 in embryonic carcinoma cells.
This study identified a critical role of the Sall4-Gli3 system at the early steps of limb development for proper development of the appendicular skeletal elements.
Sall4 also interacts with Baf60a, a member of the SWI/SNF (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 LSD1 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 and Sox2
SALL4 and KLF5 were aberrantly expressed in the CDX1(+) intestinal metaplasia of the stomach. Sustained expression of CDX1 gave rise to the induction of early intestinal-stemness markers, followed by the expression of intestinal-differentiation markers.
Taking into account the importance of SALL4 for mouse development, we conclude that SALL4 may play an important role during mammalian germ cell development.
Plzf antagonizes Sall4 function by displacing Sall4 from cognate chromatin to induce Sall1 expression
This work provides further support that Sall4 manipulation may be a new model for expanding clinically transplantable stem cells.
these data suggest that miR-103, miR-195, and miR-15b post-transcriptionally downregulated the expression of SALL4 and suppressed glioma cell growth, migration, and invasion, and increased cell apoptosis.
the role of Spalt like protein 4 (SALL4) in pancreatic ductal adenocarcinoma cell proliferation, mobility and its regulation in mitochondrial ROS via FoxM1/Prx III axis.
an HBV-pSTAT3-SALL4-miR-200c axis regulates PD-L1 causing T cell exhaustion
the TRIM21 knockdown increases SALL1 levels, indicating that TRIM21 degrades both SALL1 and SALL4.
These data indicate that aberrantly expressed SALL4 in human choriocarcinoma cells may promote cell proliferation via beta-catenin/c-Myc pathway
SALL4 was significantly upregulated in glioma tissues and cell lines, and an inverse correlation between miR-98 and SALL4 expression in glioma tissues was identified.
TNFSF13, SPATC1L, SLC22A25 and SALL4 may thus be novel susceptibility loci for atrial fibrillation in the Japanese population
Study showed significantly high expression of SALL4 mRNA in glioma specimens as compared to non-tumor samples using RT-PCR. Blocking SALL4 using SALL4-siRNA decreased proliferation of U87 and U251 cells, which was reversed by the addition of PTEN inhibitor phen (bpv). Furthermore, marked increase in PTEN mRNA and protein levels was seen in cells treated with siRNA-SALL4.
SALL4 is a promising prognostic biomarker for cancer, and is appropriate for the assessment of cancer prognosis in the Chinese people.
Our experimental data indicated that over expression of SALL4 was found in CRC and low expression of SALL4 was connected with high survival rate after surgery. Thus our study suggested that SALL4 could serve as a potential diagnostic and prognostic marker of CRC.
SALL4 is a target gene of miR-181b in glioma.SALL4 is upregulated in glioma.
SALL4 is a target gene of mir-98 in non-small cell lung cancer cells.
miR-98 plays a suppressive role in the proliferation, migration, invasion and EMT of HCC cells, partly at least, via directly inhibition of SALL4.
SALL4 immunopositivity is not a prognostic factor in Combined hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC) (cHCC-CC); however, it is associated with alpha-fetoprotein, glypican 3 and EpCAM immunopositivity, indicating the mechanism of carcinogenesis.
these data suggest that Bmi-1 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 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 (MST1/2)/YAP signaling, and that inhibition of miR-181a using a microRNA sponge inhibitor resulted in decreased transcription of SOX2 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 and open chromatin through a HP1alpha-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