Recombinant Human Thrombospondin-4 (THBS4), Truncated

Uniprot Id

P35443

Target Species

Human

Target Name

THBS4

Target Full Name

Thrombospondin-4

Target Function

Adhesive glycoprotein that mediates cell-to-cell and cell-to-matrix interactions and is involved in various processes including cellular proliferation, migration, adhesion and attachment, inflammatory response to CNS injury, regulation of vascular inflammation and adaptive responses of the heart to pressure overload and in myocardial function and remodeling. Binds to structural extracellular matrix (ECM) proteins and modulates the ECM in response to tissue damage, contributing to cardioprotective and adaptive ECM remodeling. Plays a role in ER stress response, via its interaction with the activating transcription factor 6 alpha (ATF6) which produces adaptive ER stress response factors and protects myocardium from pressure overload. May contribute to spinal presynaptic hypersensitivity and neuropathic pain states after peripheral nerve injury. May play a role in regulating protective astrogenesis from the subventricular zone (SVZ) niche after injury in a NOTCH1-dependent manner.

Target Subcellular Location

Endoplasmic reticulum. Sarcoplasmic reticulum. Secreted. Secreted, extracellular space. Secreted, extracellular space, extracellular matrix.

Target Protein Families

Thrombospondin family

Target Synonyms

Thbs4; thrombospondin 4; thrombospondin 4b; Thrombospondin IV; Thrombospondin-4; TSP4; TSP4_HUMAN

Target Background

The protein encoded by this gene belongs to the thrombospondin protein family. Thrombospondin family members are adhesive glycoproteins that mediate cell-to-cell and cell-to-matrix interactions. This protein forms a pentamer and can bind to heparin and calcium. It is involved in local signaling in the developing and adult nervous system, and it contributes to spinal sensitization and neuropathic pain states. This gene is activated during the stromal response to invasive breast cancer. It may also play a role in inflammatory responses in Alzheimer's disease. Alternative splicing results in multiple transcript variants.