ArticleNature communications2019
Acetyl-CoA flux regulates the proteome and acetyl-proteome to maintain intracellular metabolic crosstalk.
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Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37citing papers in PubMed
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37 citing papers in PubMed, 50 citations in OpenAlex.
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- Pharmacological Inhibition of SLC33A1 Promotes Endoplasmic Reticulum Hyperoxidation and Induces Adaptive IRE1/XBP1s Signaling.bioRxiv : the preprint server for biology · 2026Article
- Nutrients and Metabolites as Signalling Molecules in Osteoclasts.Current osteoporosis reports · 2026Review
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- Acetyl-CoA availability regulates neuronal metabolism, growth, and synaptic activity.bioRxiv : the preprint server for biology · 2026Article
- ACSS1 co-opts acetyl-CoA metabolism to drive DNA repair and undermine radiotherapy efficacy in breast cancer.Cell death & disease · 2025Article
- Direct connexin-26 interactions with membrane proteins functionally relevant to the cochlea.Human genetics · 2025Article
- Identification of the putative regulatory regions and candidate genes associated with backfat thickness and intramuscular fat content traits in Xiang pigs.BMC genomics · 2025Article
- Transporters in vitamin uptake and cellular metabolism: impacts on health and disease.Life metabolism · 2025Review
- Mechanistic insights into the acetyl-CoA recognition by SLC33A1.Cell discovery · 2025Article
- Lysine acetylation and its role in the pathophysiology of acute pancreatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Cpt1a Drives primed-to-naïve pluripotency transition through lipid remodeling.Communications biology · 2024Article
- Restoration of HMGCS2-mediated ketogenesis alleviates tacrolimus-induced hepatic lipid metabolism disorder.Acta pharmacologica Sinica · 2024Article
- Glutamine Metabolism and Prostate Cancer.Cancers · 2024Review
- Article
- The citrate transporters SLC13A5 and SLC25A1 elicit different metabolic responses and phenotypes in the mouse.Communications biology · 2023Article
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Authors and funding
15 authors at 1 institution in 1 country.
Inca A DieterichDepartment of Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Alexis J LawtonDepartment of Biomolecular Chemistry and the Wisconsin Institute for Discovery, University of Wisconsin-Madison, Madison, WI, USA.ORCID http://orcid.org/0000-0002-1065-0846
Yajing PengDepartment of Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Qing YuSchool of Pharmacy and Department of Chemistry, University of Wisconsin-Madison, Madison, WI, USA.
Timothy W RhoadsDepartment of Medicine, University of Wisconsin-Madison, Madison, WI, USA.ORCID http://orcid.org/0000-0001-7364-1122
Katherine A OvermyerDepartment of Chemistry, Biomolecular Chemistry and Genome Center of Wisconsin, University of Wisconsin-Madison, Madison, WI, USA.ORCID http://orcid.org/0000-0002-1929-1229
Yusi CuiSchool of Pharmacy and Department of Chemistry, University of Wisconsin-Madison, Madison, WI, USA.
Eric A ArmstrongDepartment of Biomolecular Chemistry and the Wisconsin Institute for Discovery, University of Wisconsin-Madison, Madison, WI, USA.
Porsha R HowellDepartment of Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Maggie S BurhansDepartment of Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Lingjun LiSchool of Pharmacy and Department of Chemistry, University of Wisconsin-Madison, Madison, WI, USA.ORCID http://orcid.org/0000-0003-0056-3869
John M DenuDepartment of Biomolecular Chemistry and the Wisconsin Institute for Discovery, University of Wisconsin-Madison, Madison, WI, USA.
Joshua J CoonDepartment of Chemistry, Biomolecular Chemistry and Genome Center of Wisconsin, University of Wisconsin-Madison, Madison, WI, USA.
Rozalyn M AndersonDepartment of Medicine, University of Wisconsin-Madison, Madison, WI, USA.
Luigi PuglielliDepartment of Medicine, University of Wisconsin-Madison, Madison, WI, USA. lp1@medicine.wisc.edu.ORCID http://orcid.org/0000-0003-0259-8424
University of Wisconsin–Madison · US
Funding
TR&D 2 Metabolic Labels for Ultraplexed Protein Quantification p. 453P41GM108538 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI COON, JOSHUA J · 2016 to 2025
$13.1MBiology of Aging and Age-Related Diseases Training GrantT32AG000213 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Rozalyn M. Anderson, Sanjay Asthana · 1991 to 2026
$9.9MNEUROSCIENCE TRAINING PROGRAMT32GM007507 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI HALLORAN, MARY C · 1985 to 2017
$9.3MReversible protein acetylation and sirtuin functionR01GM065386 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI DENU, JOHN M · 2003 to 2022
$7.3MMass Spectrometric Studies of Neuropeptides in FeedingR01DK071801 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI LINGJUN LI · 2006 to 2026
$6.7MWaisman Intellectual and Developmental Disabilities Research Center Down Syndrome RegistryU54HD090256 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI POLLAK, SETH D · 2016 to 2020
$6.0MSpastic paraplegia, neurodegeneration and autism: possible role for AT- 1/SLC33A1?R01NS094154 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI Luigi Puglielli · 2015 to 2026
$4.3MAcetyl-CoA flux and mitochondrial adaptation: a pathogenic role in aging and AD?RF1AG057408 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI ANDERSON, ROZALYN M., PUGLIELLI, LUIGI · 2017 to 2017
$3.5MDi-Leu-enabled multiplexed quantitation for biomarker discovery and validation in Alzheimer's diseaseRF1AG052324 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI LI, LINGJUN · 2018 to 2018
$2.4MDiLeu-enabled multiplexed quantitation for biomarker discovery and validation in Alzheimer’s diseaseR01AG052324 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI LINGJUN LI · 2023 to 2026
$2.3MAcquisition of a High-Field Dual Source FTICR-MS for Pharmaceutical ResearchS10RR029531 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI LI, LINGJUN · 2011 to 2011
$2.1MProteostasis in the aging and Alzheimer's disease brain: are the ATases novel targets?RF1AG053937 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI PUGLIELLI, LUIGI · 2016 to 2016
$1.9MNCRR NIH HHS S10 RR029531NIA NIH HHS R01 AG052324NIA NIH HHS RF1 AG052324NIA NIH HHS RF1 AG053937NIA NIH HHS RF1 AG057408NIA NIH HHS T32 AG000213NICHD NIH HHS U54 HD090256NIDDK NIH HHS R01 DK071801NIGMS NIH HHS P41 GM108538NIGMS NIH HHS R01 GM065386NIGMS NIH HHS T32 GM007507NINDS NIH HHS R01 NS094154
Abstract
AT-1/SLC33A1 is a key member of the endoplasmic reticulum (ER) acetylation machinery, transporting acetyl-CoA from the cytosol into the ER lumen where acetyl-CoA serves as the acetyl-group donor for Nε-lysine acetylation. Dysfunctional ER acetylation, as caused by heterozygous or homozygous mutations as well as gene duplication events of AT-1/SLC33A1, has been linked to both developmental and degenerative diseases. Here, we investigate two models of AT-1 dysregulation and altered acetyl-CoA flux: AT-1
Indexed as
Lipid MetabolismAcetylationAcetyl Coenzyme AAnimalsCytosolEndoplasmic ReticulumHaploinsufficiencyLiverLysineMembrane Transport ProteinsMice, KnockoutMice, TransgenicProteomeProteomicsAcetyl Coenzyme ALysineMembrane Transport ProteinsProteomeSlc33a1 protein, mouse
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.