Mar 30, 2025 · SMAD5 (SMAD Family Member 5) is a Protein Coding gene. Diseases associated with SMAD5 include Fibrodysplasia Ossificans Progressiva and Pulpitis. Among its related pathways are TGF-beta receptor signaling in skeletal dysplasias and TGF-Beta Pathway.

Smads (or SMADs) comprise a family of structurally similar proteins that are the main signal transducers for receptors of the transforming growth factor beta (TGF-B) superfamily, which are critically important for regulating cell development and growth.

SMAD5, as its name describes, is a homolog of the Drosophila gene: "Mothers against decapentaplegic", based on a tradition of such unusual naming within the gene research community. [6] It belongs to the SMAD family of proteins, which …

Nov 22, 2024 · Smad5 (small mothers against decapentaplegic 5) protein is a receptor-regulated member of the Smad family proteins, mainly participating in the bone morphogenetic protein (BMP) signaling pathway in its phosphorylated form.

Eight SMAD proteins are encoded by human and mouse genomes. Of these, SMAD1, SMAD2, SMAD3, SMAD5, and SMAD8 act as substrates for the TGF-β family receptor, and these proteins are commonly referred to as receptor-regulated SMADs (R-SMADs).

Jul 4, 2017 · Here we show that Smad5, a well-characterized downstream component of bone morphogenetic protein (BMP) signaling responds to pHi changes.

Aug 15, 2017 · SMADs are essential transcriptional effectors of transforming growth factor-β (TGFβ)/TGFβ-related signaling that underlies embryonic development and adult homeostasis.

We identified SMAD5 as direct target of miR-145, the suppressed expression of which consequently led to increased cell proliferation and migration/invasion. Smad5 acts as a intracellular pH messenger and maintains the bioenergetic homeostasis of cells by regulating cytoplasmic metabolic machinery.

Feb 8, 2025 · Smad5 determines murine amnion fate through the control of bone morphogenetic protein expression and signalling levels; Association of runx2 with smad 5 is essential for osteogenic induction of C2C12 cells; overexpression of Smurf1 specifically promotes Smad1 and Smad5 ubiquitination and degradation in embryonic lung epithelium

Recent investigation reveals Smad5 as a negative regulator of embryonic hematopoiesis in a haploinsufficiency fashion, helping to elucidate the cytogenetic mechanism, by which Smad5 acts as leukemia suppressor.