ArticleDiabetologia2017
A Tbc1d1
Article in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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.
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.
Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- TBC1D1 functions as a negative regulator of satellite cells for muscle regeneration.Nature communications · 2025Article
- Nuclear entry of AS160 as a transcriptional regulator of satellite cells for muscle regeneration.Nature communications · 2025Article
- Mechanism and cellular actions of the potent AMPK inhibitor BAY-3827.Science advances · 2025Article
- TBC1D1 is an energy-responsive polarization regulator of macrophages via governing ROS production in obesity.Science China. Life sciences · 2024Article
- Fine-tuning AMPK in physiology and disease using point-mutant mouse models.Disease models & mechanisms · 2024Review
- AMPK and Beyond: The Signaling Network Controlling RabGAPs and Contraction-Mediated Glucose Uptake in Skeletal Muscle.International journal of molecular sciences · 2024Review
- Is 14-3-3 the Combination to Unlock New Pathways to Improve Metabolic Homeostasis and β-Cell Function?Diabetes · 2023Review
- New insights into activation and function of the AMPK.Nature reviews. Molecular cell biology · 2023Review
- Greater Phosphorylation of AMPK and Multiple AMPK Substrates in the Skeletal Muscle of 24-Month-Old Calorie Restricted Compared to Ad-Libitum Fed Male Rats.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- The Integration of Proteome-Wide PTM Data with Protein Structural and Sequence Features Identifies Phosphorylations that Mediate 14-3-3 Interactions.Journal of molecular biology · 2023Article
- Rab2A regulates the progression of nonalcoholic fatty liver disease downstream of AMPK-TBC1D1 axis by stabilizing PPARγ.PLoS biology · 2022Article
- Prior AICAR induces elevated glucose uptake concomitant with greater γ3-AMPK activation and reduced membrane cholesterol in skeletal muscle from 26-month-old rats.Facets (Ottawa) · 2022Article
- Compound- and fiber type-selective requirement of AMPKγ3 for insulin-independent glucose uptake in skeletal muscle.Molecular metabolism · 2021Article
- The PPARβ/δ-AMPK Connection in the Treatment of Insulin Resistance.International journal of molecular sciences · 2021Review
- AMPK-dependent and -independent coordination of mitochondrial function and muscle fiber type by FNIP1.PLoS genetics · 2021Article
- Inducible deletion of skeletal muscle AMPKα reveals that AMPK is required for nucleotide balance but dispensable for muscle glucose uptake and fat oxidation during exercise.Molecular metabolism · 2020Article
- In vivo glucoregulation and tissue-specific glucose uptake in female Akt substrate 160 kDa knockout rats.PloS one · 2020Article
- Targeting RalGAPα1 in skeletal muscle to simultaneously improve postprandial glucose and lipid control.Science advances · 2019Article
- Review
- AMPK in skeletal muscle function and metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisTBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) is a Rab GTPase-activating protein (RabGAP) that has been implicated in regulating GLUT4 trafficking. TBC1D1 can be phosphorylated by the AMP-activated protein kinase (AMPK) on Ser
methodsWhole-body glucose homeostasis and muscle glucose uptake were assayed in mice bearing a Tbc1d1
resultsSkeletal muscle-specific deletion of Ampkα1/a2 in mice prevented AICAR-induced hypoglycaemia and muscle glucose uptake. The Tbc1d1 CONCLUSIONS/
interpretationTBC1D1-Ser
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What OpenQuestion holds
Registered trials
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.