Evidence map›Paper›PMID 34245780›Full record

ArticleThe Journal of biological chemistry2021

The innate immune kinase TBK1 directly increases mTORC2 activity and downstream signaling to Akt.

Aaron Seth Tooley, Dubek Kazyken, Cagri Bodur, Ian E Gonzalez, Diane C Fingar

Open access · goldAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Viral Modulation of Host Splicing.Annual review of virology · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Role of TBK1 Inhibition in Targeted Therapy of Cancer.Mini reviews in medicinal chemistry · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The role of TBK1 in cancer pathogenesis and anticancer immunity.Journal of experimental & clinical cancer research : CR · 2022
    Review
  18. Article
  19. TBK1 has a new Akt.The Journal of biological chemistry · 2021
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Aaron Seth TooleyDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Dubek KazykenDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Cagri BodurDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Ian E GonzalezDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Diane C FingarDepartment of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan, USA. Electronic address: dfingar@umich.edu.
University of Michigan · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Cellular Biotechnology Training Program (CBTP) - Years 31-35T32GM145304 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Guizhi Zhu · 2022 to 2026
$2.6M
Unexpected role for AMPK and mTORC1 in cellular adaptation to nutrient stressR01GM137577 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FINGAR, DIANE C. · 2021 to 2024
$1.4M
Direct regulation of mTORC1 and mTORC2 by the IKK-related kinases TBK1 and IKKϵR01DK103877 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FINGAR, DIANE C. · 2014 to 2017
$838k
Integration of innate immune function and metabolism by the TBK1-mTOR axisR56DK126328 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FINGAR, DIANE C. · 2020 to 2020
$156k
NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK103877NIDDK NIH HHS R56 DK126328NIGMS NIH HHS R01 GM137577NIGMS NIH HHS T32 GM145304
6 · The paper itself

Abstract

TBK1 responds to microbes to initiate cellular responses critical for host innate immune defense. We found previously that TBK1 phosphorylates mTOR (mechanistic target of rapamycin) on S2159 to increase mTOR complex 1 (mTORC1) signaling in response to the growth factor EGF and the viral dsRNA mimetic poly(I:C). mTORC1 and the less well studied mTORC2 respond to diverse cues to control cellular metabolism, proliferation, and survival. Although TBK1 has been linked to Akt phosphorylation, a direct relationship between TBK1 and mTORC2, an Akt kinase, has not been described. By studying MEFs lacking TBK1, as well as MEFs, macrophages, and mice bearing an Mtor S2159A knock-in allele (Mtor

Indexed as

Mechanistic Target of Rapamycin Complex 2Protein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsHEK293 CellsHumansImmunity, InnateMicePhosphorylationTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 2Protein Serine-Threonine KinasesProto-Oncogene Proteins c-aktTBK1 protein, humanTbk1 protein, mouseTOR Serine-Threonine KinasesAktmTORmTORC2phosphorylationTBK1

Identifiers

PMID34245780
PMCPMC8342794
OpenAlexW3142867995

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.