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anti-Mouse (Murine) RERE Antibodies:
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Results suggest that atrophin2 plays a role in the feedback regulation of Fgf8 signaling.
the Atro-Rpd3 complex plays a conserved role to function as a Ci(R) corepressor.
Tissue-specific transcriptional repression, by means of an REREa-Histone Deacetylase complex, modulates growth factor signaling during embryogenesis.
Rere and Gata4 interact genetically in the development of congenital heart defects.
RERE-deficiency leads to delayed development of the principal fissures and delayed maturation and migration of Purkinje cells, abnormal cerebellar foliation and Purkinje cell maturation during postnatal cerebellar development.
RERE plays a critical role in the development.
a mutation in Rere (also known as atrophin2) leads to the formation of asymmetrical somites in mouse embryos, similar to embryos deprived of retinoic acid
act as transcriptional co-repressor during embryonic development.
Atrophin-1 and the short form of Atrophin-2 can act as potent and evolutionarily conserved transcriptional activators.
suggest that mutations in RERE cause a genetic syndrome and that haploinsufficiency of RERE might be sufficient to cause many of the phenotypes associated with proximal 1p36 deletions
The mouse ortholog of RERE is required for embryonic development
This gene encodes a member of the atrophin family of arginine-glutamic acid (RE) dipeptide repeat-containing proteins. The encoded protein co-localizes with a transcription factor in the nucleus, and its overexpression triggers apoptosis. A similar protein in mouse associates with histone deacetylase and is thought to function as a transcriptional co-repressor during embryonic development. Multiple transcript variants encoding different isoforms have been found for this gene.
, gaping mouth
, arginine-glutamic acid dipeptide (RE) repeats
, atrophin-1 like protein
, arginine-glutamic acid dipeptide repeats protein
, atrophin-1 related protein
, atrophin-1-like protein
, atrophin-1-related protein