Author

M. J. Lazzara

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Biochemistry· 1 Cancer Biology· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell signaling & trafficking· 3 Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Organism:human· 2 Assay:proteomics· 2 Research Focus:cell type annotation· 1 Assay:ChIP-seq· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

A. K. Solanki· 1 shared A. Singh· 1 shared B. A. Brown· 1 shared B. Rahman· 1 shared B. W. Berger· 1 shared B. Z. Stanger· 1 shared C. M. Furcht· 1 shared D. Nihalani· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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1 shared paperCell Biology

A. K. Solanki

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

A histone methylation-MAPK signaling axis drives durable epithelial-mesenchymal transition in hypoxic pancreas cancer

B. A. Brown, P. J. Myers, S. J. Adair, J. R. Pitarresi, S. K. Sah-Teli, L. A. Campbell, W. S. Hart, M. Barbeau, K. Leong, N. Seyler, W. Kane, K. E. Lee, E. Stelow, M. Jones, M. C. Simon, , M. J. Lazzara

This study identifies a hypoxia-driven histone methylation-MAPK feedback loop that sustains EMT in pancreatic cancer, with potential therapeutic implications.

bioRxiv · Oct 19, 2022 · PreprintCancer Biology

HGF-induced activation of NEPHRIN and NEPH1 serves as a novel mechanism for recovery of podocytes from injury

A. K. Solanki, P. Srivastava, E. Arif, C. M. Furcht, B. Rahman, P. Wen, A. Singh, L. B. Holzman, W. R. Fitzgibbon, G. Lobo, J. H. Lipschutz, S.-H. Kwon, Z. Han, M. J. Lazzara, D. Nihalani

This study identifies HGF as a ligand that activates NEPHRIN and NEPH1 through direct binding, promoting podocyte recovery from injury.

bioRxiv · May 4, 2020 · PreprintCell Biology

Disrupting the Transmembrane Domain Oligomerization of Protein Tyrosine Phosphatase Receptor J Promotes its Activity in Cancer Cells

E. Bloch, E. Sikorski, D. Pontoriero, B. W. Berger, M. J. Lazzara, D. Thevenin

This study shows that disrupting the transmembrane domain oligomerization of PTPRJ enhances its activity, reduces EGFR phosphorylation, and promotes substrate access in cancer cells.

bioRxiv · Oct 7, 2019Biochemistry