SALL2 is a multi-zinc finger transcription factor belonging to the Drosophila homeotic spalt-like family of developmental transcription factor genes. It is expressed during the development of human retina at the time of optic fissure closure.
Immunogen
SALL2 (ENSP00000320536, 1 a.a. ~ 198 a.a) full-length human protein.
SALL2 mainly associated with the growth arrest and pro-apoptotic functions. It is involved in eye morphogenesis. Alteration in the gene function causes ocular coloboma in humans and mice. It has ability to supress the c-MYC transcription by binding to the nuclease hypersensitive element of the c-MYC promoter.
p150, product of the SALL2 gene, is a binding partner of the polyoma virus large T antigen and a putative tumor suppressor. p150 binds to the nuclease hypersensitive element of the c-MYC promoter and represses c-MYC transcription. Overexpression of p150
Biochimica et biophysica acta, 1809(4-6), 276-283 (2011-03-03)
The product of the SALL2 protein p150(Sal2) is a multi-zinc finger transcription factor with growth arrest and proapoptotic functions that overlap those of p53. Its DNA-binding properties are unknown. We have used a modified SELEX procedure with purified p150(Sal2) and
Human molecular genetics, 23(10), 2511-2526 (2014-01-15)
Ocular coloboma is a congenital defect resulting from failure of normal closure of the optic fissure during embryonic eye development. This birth defect causes childhood blindness worldwide, yet the genetic etiology is poorly understood. Here, we identified a novel homozygous
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