|1.||Starr, Mark D: 1 article (06/2014)|
|2.||Gatza, Catherine E: 1 article (06/2014)|
|3.||Elderbroom, Jennifer L: 1 article (06/2014)|
|4.||Nixon, Andrew B: 1 article (06/2014)|
|5.||Oh, Sun Young: 1 article (06/2014)|
|6.||Blobe, Gerard C: 1 article (06/2014)|
|7.||Nakahata, Norimichi: 1 article (12/2009)|
|8.||Uchiyama, Kotomi: 1 article (12/2009)|
|9.||Obara, Yutaro: 1 article (12/2009)|
|10.||Saito, Masaki: 1 article (12/2009)|
07/01/2005 - "In vivo treatment with the hydroxamate-based metalloprotease inhibitors BB3103 or TAPI-2 (tumour necrosis factor-alpha protease inhibitor 2) reversibly induced accumulation of forms of proTGFalpha that included the N-terminal extension. "
03/01/2004 - "Hmeprin is inhibited by hydroxamic acid derivatives such as batimastat, galardin and Pro-Leu-Gly-hydroxamate, by TAPI-0 (tumour necrosis factor alpha protease inhibitor-0) and TAPI-2, and by thiol-based compounds such as captopril. "
|2.||Breast Neoplasms (Breast Cancer)
06/01/2014 - "Inhibition of TβRIII shedding through treatment with TAPI-2 or expression of a non-shedding TβRIII mutant rescued TβRIII mediated inhibition of BMP induced Smad1/5/8 phosphorylation and BMP induced migration and/or invasion in both in normal mammary epithelial cells and breast cancer cells. "
|3.||Astrocytoma (Pilocytic Astrocytoma)
12/08/2009 - "A TP agonist U46619 caused the phosphorylation of EGFR in 1321N1 human astrocytoma cells, which was inhibited by an EGFR selective inhibitor AG1478 and by a disintegrin and metalloproteinase (ADAM) inhibitor TAPI-2, indicating TP stimulation caused the EGFR transactivation through the EGFR ligand shedding. "
|1.||Protease Inhibitors (Protease Inhibitor)
|2.||15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
|3.||Hydroxamic Acids (Hydroxamic Acid)
|5.||tyrphostin AG 1478
|7.||batimastat (BB 94)