EC Number   |
General Information |
Reference |
|---|
  3.4.21.122 | drug target |
TMPRSS2 is a secreted protease that is highly expressed in prostate and prostate cancer, making it a potential target for cancer therapy and diagnosis |
764399 |
| 3.4.21.122 | malfunction |
TMPRSS2 knockdown in cultured human airway epithelial cells (H441) reduces baseline proteolytic activation of endogenously expressed epithelial sodium channel (ENaC) |
765086 |
| 3.4.21.122 | metabolism |
angiotensin-converting enzyme-2 (ACE2) and the transmembrane serine protease 2 (TMPRSS2) seem to be positively related to IFN-gamma and TNF-alpha production in chronic rhinosinusitis patient. ACE2 and TMPRSS2 are co-expressed in the ciliated epithelium of their paranasal mucosa, implicating the paranasal epithelium as a portal for initial infection and transmission |
763869 |
| 3.4.21.122 | physiological function |
ACE2 processing by TMPRSS2 or HAT is required for augmentation of SARS-S-driven entry. In contrast, ACE2 cleavage is dispensable for activation of the viral S protein. Expression of TMPRSS2 increases cellular uptake of soluble SARS-S. TMPRSS2 competes with the metalloprotease ADAM17 for ACE2 processing, but only cleavage by TMPRSS2 results in augmented SARS-S-driven entry |
754540 |
| 3.4.21.122 | physiological function |
acute oxidative stress leads to redistribution of TMPRSS2 from cell membrane to cytoplasm in IPEC-J2 cells |
753810 |
| 3.4.21.122 | physiological function |
after experimental infectionusing MERS coronavirus, TMPRSS2-deficient mouse strains show reduced body weight loss and viral kinetics in the lungs. Lack of TMPRSS2 affects the primary sites of infection and virus spread within the airway, accompanied by less severe immunopathology. TMPRSS2-KO mice show weakened inflammatory chemokine and/or cytokine responses to intranasal stimulation with poly(IC), a Toll-like receptor 3 agonist |
754560 |
| 3.4.21.122 | physiological function |
after infection of Tmprss2 knockout mice with an H3N2 influenza virus, only a slight increase in survival is observed. Tmprss2-/- Tmprss4-/-x02double-knockout mice show a remarkably reduced virus spread and lung pathology, in addition to reduced body weight loss and mortality |
754551 |
| 3.4.21.122 | physiological function |
angiotensin-converting enzyme ACE2 and TMPRSS2 colocalize on cell surfaces and enhance the cell entry of both SARS S-pseudotyped HIV and authentic SARS-CoV. Enhanced entry correlates with TMPRSS2-mediated proteolysis of both S protein and ACE2 |
754533 |
| 3.4.21.122 | physiological function |
both proteases HAT and TMPRSS2 are coexpressed with 2,6-linked sialic acids, the major receptor determinant of human influenza viruses, throughout the human respiratory tract. Coexpression of ACE2 and TMPRSS2 is frequently found in the upper and lower aerodigestive tract, with the exception of the vocal folds, epiglottis and trachea. Activation of influenza virus is conserved between human, avian and porcine TMPRSS2 |
755193 |
| 3.4.21.122 | physiological function |
compared to wild-type littermates, Tmprss2-/- mice develop normally, survive to adulthood with no differences in protein levels of prostatic secretions, and exhibit no discernible abnormalities in organ histology or function. Loss of TMPRSS2 activity does not influence fertility, reduce survival, result in prostate hyperplasia or carcinoma, or alter prostatic luminal epithelial cell regrowth following castration and androgen replacement |
754724 |
