Evidence map›Paper›PMID 33785595›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Selective autophagy of AKAP11 activates cAMP/PKA to fuel mitochondrial metabolism and tumor cell growth.

Zhiqiang Deng, Xianting Li, Marian Blanca Ramirez, Kerry Purtell, Insup Choi, Jia-Hong Lu, Qin Yu, Zhenyu Yue

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 57 citations in OpenAlex.

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  15. Turning garbage into gold: Autophagy in synaptic function.Current opinion in neurobiology · 2025
    Review
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4 · The record

Corrections and comments

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

8 authors at 3 institutions in 2 countries.

Zhiqiang DengDepartment of Neurology, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Xianting LiDepartment of Neurology, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Marian Blanca RamirezDepartment of Neurology, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Kerry PurtellDepartment of Neurology, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Insup ChoiDepartment of Neurology, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
Jia-Hong LuState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, 999078 Macau SAR, China.
Qin YuDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029.ORCID 0000-0003-1736-7338
Zhenyu YueDepartment of Neurology, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029; zhenyu.yue@mssm.edu.
Allen Institute for Brain Science · USIcahn School of Medicine at Mount Sinai · USUniversity of Macau · MO

Funding

Neuronal Autophagy: a Cell-Autonomous Protection MechanismR01NS060123 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Zhenyu Yue · 2008 to 2026
$9.2M
Mouse CoreP50NS094733 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2015 to 2020
$7.1M
Developing therapeutics against resistance to the androgen-deprivation therapyR01CA200611 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI YU, QIN · 2016 to 2020
$1.9M
CD44 Antagonists in Targeted and Combinational Therapy for GlioblastomaR01CA150355 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI YU, QIN · 2010 to 2015
$1.7M
Merlin Signal in Glioma: Therapeutic Agents and TargetsR01CA135158 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI YU, QIN · 2009 to 2010
$698k
NCI NIH HHS R01 CA135158NCI NIH HHS R01 CA150355NCI NIH HHS R01 CA200611NINDS NIH HHS P50 NS094733NINDS NIH HHS R01 NS060123
6 · The paper itself

Abstract

Autophagy is a catabolic pathway that provides self-nourishment and maintenance of cellular homeostasis. Autophagy is a fundamental cell protection pathway through metabolic recycling of various intracellular cargos and supplying the breakdown products. Here, we report an autophagy function in governing cell protection during cellular response to energy crisis through cell metabolic rewiring. We observe a role of selective type of autophagy in direct activation of cyclic AMP protein kinase A (PKA) and rejuvenation of mitochondrial function. Mechanistically, autophagy selectively degrades the inhibitory subunit RI of PKA holoenzyme through A-kinase-anchoring protein (AKAP) 11. AKAP11 acts as an autophagy receptor that recruits RI to autophagosomes via LC3. Glucose starvation induces AKAP11-dependent degradation of RI, resulting in PKA activation that potentiates PKA-cAMP response element-binding signaling, mitochondria respiration, and ATP production in accordance with mitochondrial elongation. AKAP11 deficiency inhibits PKA activation and impairs cell survival upon glucose starvation. Our results thus expand the view of autophagy cytoprotection mechanism by demonstrating selective autophagy in RI degradation and PKA activation that fuels the mitochondrial metabolism and confers cell resistance to glucose deprivation implicated in tumor growth.

Indexed as

AutophagyA Kinase Anchor ProteinsAnimalsCyclic AMPCyclic AMP-Dependent Protein KinasesHCT116 CellsHEK293 CellsHeLa CellsHumansMiceMitochondriaNeoplasmsAKAP11 protein, humanA Kinase Anchor ProteinsCyclic AMPCyclic AMP-Dependent Protein KinasesAKAP11autophagycell survivalmitochondrial metabolismPKA

Identifiers

PMID33785595
PMCPMC8040602
OpenAlexW3151202750

What OpenQuestion holds

Textmetadata
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.