Cole M. Haynes

University of Massachusetts Chan Medical School — United States

Biochemistry, Genetics and Molecular Biology · Life Sciences

45h-index15.5kcitations91works5.12yr avg
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Research Topics

Mitochondrial Function and Pathology(51), Endoplasmic Reticulum Stress and Disease(39), Genetics, Aging, and Longevity in Model Organisms(33), Ubiquitin and proteasome pathways(12), Adipose Tissue and Metabolism(12)

Publications90 total

The ESCRT protein CHMP5 restricts bone formation by controlling endolysosome-mitochondrion-mediated cell senescence
eLife·2025Open Access
Author response: The ESCRT protein CHMP5 restricts bone formation by controlling endolysosome-mitochondrion-mediated cell senescence
2025Open Access
Multidimensional third-generation sequencing of modified DNA bases allows interrogation of complex biological systems
Nature Communications·2025· 1 citedOpen Access
The ESCRT protein CHMP5 restricts bone formation by controlling endolysosome-mitochondrion-mediated cell senescence
2025Open Access
Author response: The ESCRT protein CHMP5 restricts bone formation by controlling endolysosome-mitochondrion-mediated cell senescence
2025Open Access
AMP accumulation during mitochondrial stress induces transcription of cytosolic and mitochondrial protein synthesis components via NHR-180
2025Open Access
The ESCRT protein CHMP5 restricts bone formation by controlling endolysosome-mitochondrion-mediated cell senescence
2024Open Access
Author response: The ESCRT protein CHMP5 restricts bone formation by controlling endolysosome-mitochondrion-mediated cell senescence
2024Open Access
The ESCRT protein CHMP5 restricts bone formation by controlling endolysosome-mitochondrion-mediated cell senescence
eLife·2024· 1 citedOpen Access
Publisher Correction: Host–microbe interactions rewire metabolism in a C. elegans model of leucine breakdown deficiency
Nature Metabolism·2024Open Access
Host–microbe interactions rewire metabolism in a C. elegans model of leucine breakdown deficiency
Nature Metabolism·2024· 4 citedOpen Access
Mitochondrial inorganic polyphosphate is required to maintain proteostasis within the organelle
Frontiers in Cell and Developmental Biology·2024· 8 citedOpen Access
Regulation of proteostasis and innate immunity via mitochondria-nuclear communication
The Journal of Cell Biology·2024· 16 citedOpen Access
Itaconate impairs immune control of Plasmodium by enhancing mtDNA-mediated PD-L1 expression in monocyte-derived dendritic cells
Cell Metabolism·2024· 45 citedOpen Access
Methods to analyze the mitochondrial unfolded protein response (UPRmt)
Methods in enzymology on CD-ROM/Methods in enzymology·2024· 2 cited
ATFS-1 counteracts mitochondrial DNA damage by promoting repair over transcription
Nature Cell Biology·2023· 14 cited
The hepatic integrated stress response suppresses the somatotroph axis to control liver damage in nonalcoholic fatty liver disease
Cell Reports·2022· 18 citedOpen Access
Mitochondrial genome recovery by ATFS-1 is essential for development after starvation
Cell Reports·2022· 13 citedOpen Access
Impaired mitochondrial oxidative metabolism in skeletal progenitor cells leads to musculoskeletal disintegration
Nature Communications·2022· 34 citedOpen Access
Mitochondrial dysfunction, aging, and the mitochondrial unfolded protein response in <i>Caenorhabditis elegans</i>
Genetics·2022· 35 citedOpen Access
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Frequent Co-authors

Mark W. Pellegrino(9), David Ron(9), Amrita M. Nargund(6), Christopher J. Fiorese(6), Nandhitha Uma Naresh(5), Pengpeng Liu(5), Anna M. Schulz(4), Yifan Lin(4), Yun Yang(4), Qiyuan Yang(4), Lihua Julie Zhu(4), Antony A. Cooper(3), Brooke M. Baker(3), Tomer Shpilka(3), Thomas A. Neubert(3), Pan Deng(3), R. Luke Wiseman(3), Yunguang Du(3), Ariel Stanhill(3), Read Pukkila-Worley(3)