Author

P. Machiraju

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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Cell Biology· 3

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Approach:experimental assay· 3 Organism:human· 3 Assay:bulk RNA-seq· 2 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1 Assay:proteomics· 1

Frequent Co-Authors

F. Iqbal· 3 shared S. C. Greenway· 3 shared A. Khan· 2 shared A. Ravandi· 2 shared J. Huang· 2 shared R. Sabouny· 2 shared T. Shutt· 2 shared T. Zhao· 2 shared

Activity by Year

2019-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersCell Biology

F. Iqbal

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3 papers

Recent·Most cited

Cell BiologyCanadian Journal of CardiologyPeer-reviewedApr 1, 2020

Reversible Mitochondrial Fragmentation in iPSC-Derived Cardiomyocytes from Children with DCMA, a Mitochondrial Cardiomyopathy

L. Rohani, P. Machiraju, R. Sabouny…·S. C. Greenway

This study uses iPSC-derived cardiomyocytes from DCMA patients to show reversible mitochondrial fragmentation and OPA1 isoform imbalance, suggesting SS-31 as a potential therapy.

DOI 10.1016/j.cjca.2019.09.021

humanbulk RNA-seq

𝕏 PostBluesky

Cell BiologybioRxivPreprintNov 26, 2019

Early Inhibition of Retinoic Acid Signaling Rapidly Generates Cardiomyocytes Expressing Ventricular Markers from Human Induced Pluripotent Stem Cells

P. Machiraju, J. Huang, F. Iqbal…·S. C. Greenway

This study shows that inhibiting retinoic acid signaling early in differentiation rapidly generates ventricular-like cardiomyocytes from human iPSCs with higher MLC2V expression.

DOI 10.1101/856575

humanbulk RNA-seq

𝕏 PostBluesky

Cell BiologybioRxivJun 17, 2019

SS-31 Reverses Mitochondrial Fragmentation in Fibroblasts from Patients with DCMA, a Mitochondrial Cardiomyopathy

P. Machiraju, X. Wang, R. Sabouny…·S. C. Greenway

This study shows that SS-31 reverses mitochondrial fragmentation and increases ROS in DCMA fibroblasts, suggesting it as a potential therapy for this mitochondrial cardiomyopathy.

DOI 10.3389/fcvm.2019.00167

humanproteomics

𝕏 PostBluesky