Kayla J. Bendinelli

ORCID: 0000-0002-4072-9002
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About
Contact & Profiles
Research Areas
  • Single-cell and spatial transcriptomics
  • Protease and Inhibitor Mechanisms
  • Cell Adhesion Molecules Research
  • Blood Coagulation and Thrombosis Mechanisms
  • Receptor Mechanisms and Signaling
  • Cancer Immunotherapy and Biomarkers
  • Immunotherapy and Immune Responses
  • Congenital heart defects research
  • Peptidase Inhibition and Analysis
  • Cancer-related molecular mechanisms research
  • Gene Regulatory Network Analysis

Sidney Kimmel Comprehensive Cancer Center
2024

Johns Hopkins University
2024

Broad Institute
2021-2024

Loss-of-function mutations in the secreted enzyme ADAMTS7 (a disintegrin and metalloproteinase with thrombospondin motifs 7) are associated protection for coronary artery disease. catalytic inhibition has been proposed as a therapeutic strategy treating disease; however, lack of an endogenous substrate hindered development activity-based biomarkers. To identify extracellular substrates their cleavage sites relevant to vascular disease, we used TAILS (terminal amine isotopic labeling...

10.1016/j.mcpro.2022.100223 article EN cc-by-nc-nd Molecular & Cellular Proteomics 2022-03-11

Abstract Background Despite the critical role of cardiovascular system, our understanding its cellular and transcriptional diversity remains limited. We therefore sought to characterize composition, phenotypes, molecular pathways, communication networks between cell types at tissue sub-tissue level across system healthy Wistar rat, an important model in preclinical research. obtained high quality samples under controlled conditions that reveal a detail so far inaccessible human studies....

10.1101/2023.11.14.567085 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-11-16

Loss-of-function mutations in the secreted enzyme ADAMTS7 (a disintegrin and metalloproteinase with thrombospondin motifs 7) are associated protection for coronary artery disease (CAD). catalytic inhibition has been proposed as a therapeutic strategy treating CAD; however, lack of an endogenous substrate hindered development activity-based biomarkers. To identify extracellular substrates their cleavage sites relevant to vascular disease, we used TAILS (terminal amine isotopic labeling...

10.1101/2021.11.19.469331 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-11-19
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