Nashmil Emami1, Eleftherios P Diamandis. 1. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Abstract
BACKGROUND: The human tissue kallikrein gene family, located at chromosome 19q13.4, is the largest contiguous family of proteases in the human genome. The locus encodes all 15 members of the family, 13 of which have been reported as potential biomarkers for several carcinomas and other non-neoplastic diseases. Kallikreins are expressed by a wide range of tissues and implicated in a number of physiological functions, including skin desquamation, semen liquefaction, neural plasticity and the regulation of blood pressure. Kallikrein function is regulated at various levels, including transcription, translation and post-translation. The proteolytic activity of kallikreins is believed to be cascade mediated and may cross-talk with other proteases. These cascades are highly regulated through a series of feedback loops, inhibitors, (auto) degradation and internal cleavage. Uncontrolled proteolytic activity of kallikreins is implicated in a large number of neoplastic and non-neoplastic pathological conditions. CONCLUSIONS: As our understanding of their regulatory and functional mechanisms continues to expand, kallikreins are expected to become novel targets for the design of new therapeutics.
BACKGROUND: The human tissue kallikrein gene family, located at chromosome 19q13.4, is the largest contiguous family of proteases in the human genome. The locus encodes all 15 members of the family, 13 of which have been reported as potential biomarkers for several carcinomas and other non-neoplastic diseases. Kallikreins are expressed by a wide range of tissues and implicated in a number of physiological functions, including skin desquamation, semen liquefaction, neural plasticity and the regulation of blood pressure. Kallikrein function is regulated at various levels, including transcription, translation and post-translation. The proteolytic activity of kallikreins is believed to be cascade mediated and may cross-talk with other proteases. These cascades are highly regulated through a series of feedback loops, inhibitors, (auto) degradation and internal cleavage. Uncontrolled proteolytic activity of kallikreins is implicated in a large number of neoplastic and non-neoplastic pathological conditions. CONCLUSIONS: As our understanding of their regulatory and functional mechanisms continues to expand, kallikreins are expected to become novel targets for the design of new therapeutics.
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