Protein Flightless-1 Homolog (FLII) Antibody – Rabbit Polyclonal

This gene encodes a protein with gelsolin-like repeats and an N-terminal leucine-rich repeat domain. The protein is similar to a Drosophila protein involved in early embryogenesis and the structural organization of indirect flight muscle. This protein may act as an actin-remodelling protein as well as a transcriptional coactivator. Homozygous knockout mice show embryonic lethality. This protein may act to regulate wound repair. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Oct 2014]

FLI: May play a role as coactivator in transcriptional activation by hormone-activated nuclear receptors (NR) and acts in cooperation with NCOA2 and CARM1. Involved in estrogen hormone signaling. Involved in early embryonic development. May play a role in regulation of cytoskeletal rearrangements involved in cytokinesis and cell migration. Deletion of the FLII gene may be a cause of Smith-Magenis syndrome (SMS). It is a contiguous gene deletion syndrome involving developmental abnormalities and mental retardation. The spectrum of clinical findings includes short stature, brachydactyly, developmental delay, dysmorphic features, sleep disturbances, and behavioral problems.

Protein type: Nuclear receptor co-regulator; Actin-binding

Cellular Component: brush border; cell junction; cytoplasm; cytoskeleton; microtubule organizing center; nucleoplasm; nucleus

Molecular Function: actin binding; protein binding

Biological Process: actin cytoskeleton organization and biogenesis; actin filament severing; multicellular organismal development; regulation of transcription, DNA-dependent; transcription, DNA-dependent