Article in The Journal of cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
13 authors.
Thabata L A DuqueAutophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.ORCID 0000-0001-8922-3822
Masroor PaddarAutophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.ORCID 0009-0008-5639-3006
Einar TrosdalAutophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.ORCID 0000-0003-4637-190X
Ruheena JavedAutophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.ORCID 0000-0003-4509-6264
Lee AllersAutophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.ORCID 0000-0002-3742-6406
Michal H MuddAutophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.ORCID 0009-0002-9572-7079
Prithvi AkepatiGastroenterology Division, Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM, USA.ORCID 0009-0005-0102-9299
Soumya R MishraAutophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.ORCID 0009-0003-1954-9626
Michelle SalemiProteomics Core Facility, UC Davis Genome Center, University of California, Davis, CA, USA.ORCID 0000-0003-3990-7964
Brett PhinneyProteomics Core Facility, UC Davis Genome Center, University of California, Davis, CA, USA.ORCID 0000-0003-3870-3302
Shawn B BrattonUniversity of Texas MD Anderson Cancer Center , Houston, TX, USA.ORCID 0000-0003-2895-5020
Thomas WilemanNorwich Medical School, University of East Anglia , Norwich, UK.ORCID 0000-0002-9033-2580
Vojo DereticAutophagy, Inflammation and Metabolism Center of Biochemical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.ORCID 0000-0002-3624-5208
Funding
Unfolded Protein Response and Autophagy in T Helper Cell Effector FunctionP20GM121176 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Samuel Joseph Endicott · 2017 to 2026
$24.9M
Autophagy Against Tuberculosis and HIVR01AI111935 · NIAID · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI DERETIC, VOJO P · 2014 to 2023
$7.0M
Pattern Recognition Receptors and Autophagy in Mtb Control in AIDSR37AI042999 · NIAID · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI VOJO P DERETIC · 2018 to 2026
$4.7M
Noncanonical roles of Bim in heat shock-induced cell deathR01GM155335 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Shawn B Bratton · 2024 to 2026
The mechanisms governing mammalian proton pump V-ATPase function are of fundamental and medical interest. The assembly and disassembly of cytoplasmic V1 domain with the membrane-embedded V0 domain of V-ATPase is a key aspect of V-ATPase localization and function. Here, we show that the mammalian protein ATG16L1, primarily appreciated for its role in canonical autophagy and in noncanonical membrane atg8ylation processes, controls V-ATPase. ATG16L1 knockout elevated V-ATPase activity, increased V1 presence on endomembranes, and increased the number of acidified intracellular compartments. ATG16L1's ability to efficiently bind V-ATPase was required for its inhibitory role in endolysosomal acidification and for control of Mycobacterium tuberculosis infection in mice. These findings uncover a hitherto unappreciated role of ATG16L1 in regulating V-ATPase, a key pump governing acidification and functionality of the endolysosomal system along with its physiological roles.
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.
ATG16L1 controls mammalian vacuolar proton ATPase. · full record | OpenQuestion