Recombinant Human TIMP3 protein (GST tag N-Terminus)

Supplementary information

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

Tissue inhibitor of metalloproteinases 3 (TIMP3) is widely recognized for its role in inhibiting the activity of matrix metalloproteinases (MMPs). It has an approximate mass of 24 kDa and is often referred to by its alternate name MIG. TIMP3 is expressed in various tissues especially those involved in extracellular matrix composition such as the kidney and lungs. Its expression helps maintain the balance between matrix deposition and degradation which is critical for normal tissue homeostasis.

Biological function summary

The function of TIMP3 extends beyond mere inhibition of MMPs; it is also involved in regulating angiogenesis and apoptosis. TIMP3 forms complexes with extracellular matrix components acting as an anchor that modulates cell-matrix interactions. This capacity to bind to matrix elements enhances its inhibitory activity against proteases making it an important regulator of extracellular matrix integrity.

Pathways

TIMP3 plays significant roles in extracellular matrix remodeling and the inflammatory response. It participates in pathways involving structural organization and signaling mediation such as the NF-kB signaling cascade. TIMP3 regulates proteins like TNF-alpha and MMPs which are central to these pathways balancing inflammatory responses and tissue remodeling processes.

The imbalance of TIMP3 activity has been linked to chronic obstructive pulmonary disease (COPD) and age-related macular degeneration (AMD). In COPD impaired regulation of ECM turnover by TIMP3 leads to destructive lung tissue remodeling. In AMD the regulation of angiogenesis and degradation of ECM around the retina by TIMP3 is disturbed influencing disease progression. Its interaction with proteins such as VEGF is critical in these pathological contexts where altered TIMP3 expression or function can exacerbate disease states.