Anti-SMAD5 antibody [EPR19572-136] - BSA and Azide free (Capture)

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

SMAD5 also known as Mothers Against Decapentaplegic Homolog 5 is a protein involved in the signal transduction regulated by the transforming growth factor-beta (TGF-beta) superfamily of cytokines. This protein has a molecular mass of approximately 52 kDa and is ubiquitously expressed across various tissues. Mechanically SMAD5 functions as an intracellular mediator that translocates from the cytoplasm to the nucleus upon activation to regulate transcription. It participates actively in transmitting signals from surface receptors into the nucleus influencing gene expression.

Biological function summary

SMAD5 plays a central role in the bone morphogenetic protein (BMP) signaling pathway which is critical for embryonic development and tissue homeostasis. It forms a complex with receptor-regulated SMADs (R-SMADs) and co-SMAD (SMAD4) upon phosphorylation by BMP type I receptors. This complex then moves to the nucleus where it regulates expression of target genes. Through this mechanism SMAD5 impacts processes such as bone formation differentiation and cellular differentiation.

Pathways

Several key cellular signaling processes involve SMAD5. Primarily it contributes to the BMP pathway which is integral to skeletal development and repair. SMAD5 interacts with other SMAD proteins like SMAD1 and SMAD8 which all act downstream of the BMP receptors. Additionally SMAD5 participates in crosstalk with the TGF-beta signaling pathway enabling the fine-tuning of cellular responses to a variety of external cues. This connection places SMAD5 within a network of signaling events important for regulating different cell functions and maintaining cellular homeostasis.

Associated diseases and disorders

SMAD5's function has links to abnormal bone and cartilage development such as in fibrodysplasia ossificans progressiva (FOP) and pulmonary hypertension (PH). These conditions occur due to dysregulation within the BMP signaling pathway. For example mutations in SMAD5 or its regulatory proteins can cause inappropriate signal propagation leading to ossification in FOP or altered vascular remodeling in PH. The interplay between SMAD5 and SMAD4 another key player in these pathways highlights the complex nature of SMAD-related pathologies.