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anti-Rat (Rattus) SALL4 Antibodies:
anti-Mouse (Murine) SALL4 Antibodies:
anti-Human 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 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
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
Rat (Rattus) Polyclonal SALL4 Primary Antibody for ELISA, WB - ABIN253101
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 (show SALL1 Antibodies) 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 Antibodies) offer explanations for the similarity of individuals with Okihiro syndrome and Holt-Oram syndrome limb defects
Findings indicate that SALL4 critically contributes to MLL (show MLL Antibodies)-AF9 (show MLLT3 Antibodies)-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 (show FOXL1 Antibodies) and Dusp4 (show DUSP9 Antibodies).
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 Antibodies) and SALL4 regulatory targets in undifferentiated spermatogonia.
study explores a pivotal role of Sall4 in regulating epigenetic maturation of mouse oocytes.
JARID2 (show JARID2 Antibodies) physically interacts with ESRRB (show ESRRB Antibodies), SALL4A, and PRDM14 (show PRDM14 Antibodies)
As SALL4A is known to impair ZBTB16 (show ZBTB16 Antibodies)-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 Antibodies), Sall4 bound to these somatic cell program gene loci, which are reportedly occupied by Prdm1 (show PRDM1 Antibodies) in embryonic carcinoma cells.
This study identified a critical role of the Sall4-Gli3 (show GLI3 Antibodies) system at the early steps of limb development for proper development of the appendicular skeletal elements.
SALL4 was significantly upregulated in glioma tissues and cell lines, and an inverse correlation between miR (show MLXIP Antibodies)-98 and SALL4 expression in glioma tissues was identified.
TNFSF13 (show TNFSF13 Antibodies), SPATC1L, SLC22A25 (show SLC22A25 Antibodies) 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 (show CALR Antibodies) 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 (show CALR Antibodies).
SALL4 is a target gene of miR (show MLXIP Antibodies)-181b in glioma.SALL4 is upregulated in glioma.
SALL4 is a target gene of mir (show MLXIP Antibodies)-98 in non-small cell lung cancer cells.
miR (show MLXIP Antibodies)-98 plays a suppressive role in the proliferation, migration, invasion and EMT (show ITK Antibodies) of HCC (show FAM126A Antibodies) cells, partly at least, via directly inhibition of SALL4.
SALL4 immunopositivity is not a prognostic factor in Combined hepatocellular carcinoma (HCC (show FAM126A Antibodies)) and cholangiocarcinoma (CC) (cHCC-CC); however, it is associated with alpha-fetoprotein (show AFP Antibodies), glypican 3 (show GPC3 Antibodies) and EpCAM (show EPCAM Antibodies) immunopositivity, indicating the mechanism of carcinogenesis.
these data suggest that Bmi-1 (show BMI1 Antibodies) 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 Antibodies) could serve as a new therapeutic target for the treatment of pediatric ALL.
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