Evidence map›Paper›PMID 26880201›Full record

ArticleThe Journal of cell biology2016

Biophysical changes reduce energetic demand in growth factor-deprived lymphocytes.

Vivian C Hecht, Lucas B Sullivan, Robert J Kimmerling, Dong-Hwee Kim, Aaron M Hosios, Max A Stockslager, Mark M Stevens, Joon Ho Kang, Denis Wirtz, Matthew G Vander Heiden and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  13. Relevance and Regulation of Cell Density.Trends in cell biology · 2020
    Review
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  19. Weak protein-protein interactions in live cells are quantified by cell-volume modulation.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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

11 authors at 2 institutions in 1 country.

Vivian C HechtDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139 Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Lucas B SullivanKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.
Robert J KimmerlingDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139 Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Dong-Hwee KimJohns Hopkins Physical Sciences in Oncology Center, Johns Hopkins University, Baltimore, MD 21218 Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21218 Department of Pathology and Oncology and Sydney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD 21205.
Aaron M HosiosKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.
Max A StockslagerDepartment of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139.
Mark M StevensKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.
Joon Ho KangKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139 Department of Physics, Massachusetts Institute of Technology, Cambridge, MA 02139.
Denis WirtzJohns Hopkins Physical Sciences in Oncology Center, Johns Hopkins University, Baltimore, MD 21218 Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21218 Department of Pathology and Oncology and Sydney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD 21205.
Matthew G Vander HeidenKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139 Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139 Dana-Farber Cancer Institute, Boston, MA 02115 mvh@mit.edu srm@mit.edu.
Scott R ManalisDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139 Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139 Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139 mvh@mit.edu srm@mit.edu.
Massachusetts Institute of Technology · USSidney Kimmel Comprehensive Cancer Center · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
Interdepartmental Biotechnology Training ProgramT32GM008334 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WITTRUP, KARL DANE · 1989 to 2018
$15.2M
TRANS-NETWORK PROJECTSU54CA143874 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MANALIS, SCOTT R · 2009 to 2013
$15.1M
Regulation of glucose metabolism to allow tumor initiation and growthR01CA168653 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI VANDER HEIDEN, MATTHEW G. · 2013 to 2019
$1.9M
NCI NIH HHS P30 CA014051NCI NIH HHS P30-CA14051NCI NIH HHS R01 CA168653NCI NIH HHS U54 CA143874NCI NIH HHS U54CA143874NIGMS NIH HHS T32 GM007287NIGMS NIH HHS T32 GM008334Wellcome Trust
6 · The paper itself

Abstract

Cytokine regulation of lymphocyte growth and proliferation is essential for matching nutrient consumption with cell state. Here, we examine how cellular biophysical changes that occur immediately after growth factor depletion promote adaptation to reduced nutrient uptake. After growth factor withdrawal, nutrient uptake decreases, leading to apoptosis. Bcl-xL expression prevents cell death, with autophagy facilitating long-term cell survival. However, autophagy induction is slow relative to the reduction of nutrient uptake, suggesting that cells must engage additional adaptive mechanisms to respond initially to growth factor depletion. We describe an acute biophysical response to growth factor withdrawal, characterized by a simultaneous decrease in cell volume and increase in cell density, which occurs before autophagy initiation and is observed in both FL5.12 Bcl-xL cells depleted of IL-3 and primary CD8(+) T cells depleted of IL-2 that are differentiating toward memory cells. The response reduces cell surface area to minimize energy expenditure while conserving biomass, suggesting that the biophysical properties of cells can be regulated to promote survival under conditions of nutrient stress.

Indexed as

Energy MetabolismAdaptation, PhysiologicalAnimalsApoptosisAutophagyAutophagy-Related Protein 7bcl-X ProteinCD8-Positive T-LymphocytesCell LineIntercellular Signaling Peptides and ProteinsInterleukin-2Interleukin-3Lymphocyte ActivationLymphocytesMiceMice, TransgenicAtg7 protein, mouseAutophagy-Related Protein 7bcl-X ProteinIntercellular Signaling Peptides and ProteinsInterleukin-2Interleukin-3Microtubule-Associated Proteins

Identifiers

PMID26880201
PMCPMC4754715
OpenAlexW2282514638

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.