Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P51532 (
transcriptional activator
)
6,546
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Early in vertebrate development, endodermal signals act on mesoderm to induce cardiogenesis. The F-type SOXs
SOX7
and SOX18beta are expressed in the cardiogenic region of the early Xenopus embryo. Injection of RNAs encoding
SOX7
or SOX18beta, but not the related F-type SOX, SOX17, leads to the nodal-dependent expression of markers of cardiogenesis in animal cap explants. Injection of morpholinos directed against either
SOX7
or SOX18mRNAs lead to a partial inhibition of cardiogenesis in vivo, while co-injection of
SOX7
and SOX18 morpholinos strongly inhibited cardiogenesis.
SOX7
RNA rescued the effects of the SOX18 morpholino and visa versa, indicating that the proteins have redundant functions. In animal cap explants, it appears that
SOX7
and SOX18 act indirectly through Xnr2 to induce mesodermal (Eomesodermin, Snail, Wnt11), organizer (Cerberus) and endodermal (endodermin, Hex) tissues, which then interact to initiate cardiogenesis. Versions of
SOX7
and SOX18 with their C-terminal, beta-catenin interaction domains replaced by a
transcriptional activator
domain failed to antagonize beta-catenin activation of Siamois, but still induced cardiogenesis. These observations identify
SOX7
and SOX18 as important, and previously unsuspected, regulators of cardiogenesis in Xenopus.
...
PMID:SOX7 and SOX18 are essential for cardiogenesis in Xenopus. 1619 13