Demonstrates the Mediation of KLK-12 via the Cleavage of ECM Protein : A Part from The Book Chapter : An In-silico Study of Pathological Angiogenesis; Design of Anticancer Agent Inhibiting KLK – 12

ECM Protein

Studies show that Kallikrein like peptidase-12 (KLK-12) promotes angiogenesis through the cleavage of ECM-associated signaling proteins in the CCN family. Demonstrates the mediation of KLK-12 via the cleavage of ECM protein, Cysteine-rich angiogenic inducer 61 (CYR61) to release VEGF, FGF-2, and TGFβ from its complex to induce angiogenesis. Activation of these growth factors contributes to tumor angiogenesis. The proposed work therefore deals with the identification of new small inhibitor molecules of pathogenic angiogenesis by considering KLK-12 protein as a novel target.

Bioinformatics tools deliver a new area of personalized medicine aimed at more reliable and effective diagnosis and treatment of human diseases. This will operate in a short period of time, which will greatly increase the quality of treatment, reduce healthcare costs, precise molecular knowledge on the pathology of protein levels in diseases, and a promising potential method for healthcare system.

Author(s) Details:

Jyothi Bandi,
Department of Chemistry, University College of Science, Osmania University, Hyderabad – 500007, Telangana State, India.

Navaneetha Nambigari,
Department of Chemistry, University College of Science, Osmania University, Hyderabad – 500007, Telangana State, India and Department of Chemistry, University College of Science, Saifabad, Osmania University, Hyderabad – 500004, Telangana State, India.

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