Spalt like transcription factor 4 (SALL4) is encoded by the gene with four exons, mapped to human chromosome 20q13.13-q13.2. The encoded protein belongs to the spalt-like protein family. SALL4 is characterized with a multiple zinc finger (ZnF) domains including one N-terminal C2HC-type ZnF and seven C2H2-type ZnF domains. In vertebrates, SALL4 is abundantly expressed in both embryonic and adult stem/stem-like cells.
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). (provided by RefSeq)
Immunogen
SALL4 (NP_065169, 954 a.a. ~ 1053 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Monoclonal Anti-SALL4 antibody produced in mouse has been used in immunohistochemical staining.
Biochem/physiol Actions
Spalt like transcription factor 4 (SALL4) plays a crucial role in the regulation of cell stemness in biological development and tumor growth. Thus, this protein can be considered as a potent target for gene therapy. In addition, it also serves as a potential diagnostic marker for testicular germ cell tumors (GCTs). Polymorphisms in the gene are associated with the development of various diseases such as Duane-radial ray syndrome (DRRS, Okihiro syndrome), acro-renal-ocular syndrome (AROS), and SALL4-related Holt-Oram syndrome (HOS).
Physical form
Solution in phosphate buffered saline, pH 7.4
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RNA-binding protein LIN28 is a marker for testicular germ cell tumors
Cao D, et al.
Human Pathology, 710-8 null
Sall4 interacts with Nanog and co-occupies Nanog genomic sites in embryonic stem cells.
Wu Q, et al.
The Journal of Biological Chemistry, 24090-4 null
Multigene Deletions on Chromosome 20q13.13-q13.2 Including SALL4 Result in an Expanded Phenotype of Okihiro Syndrome Plus Developmental Delay.
Borozdin W, et al.
Human Mutation, 830 null
SALL4 Is a Novel Diagnostic Marker for Testicular Germ Cell Tumors
Cao D, et al.
American Journal of Surgical Pathology, 1065-77 null
SALL4: engine of cell stemness
Xiong J.
Current gene therapy, 400-11 null
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