PMID- 33184215
OWN - NLM
STAT- MEDLINE
DCOM- 20201209
LR  - 20211204
IS  - 1095-9203 (Electronic)
IS  - 0036-8075 (Linking)
VI  - 370
IP  - 6518
DP  - 2020 Nov 13
TI  - A phosphorylation-regulated eIF3d translation switch mediates cellular adaptation 
      to metabolic stress.
PG  - 853-856
LID - 10.1126/science.abb0993 [doi]
AB  - Shutoff of global protein synthesis is a conserved response to cellular stresses. 
      This general phenomenon is accompanied by the induction of distinct gene programs 
      tailored to each stress. Although the mechanisms driving repression of general 
      protein synthesis are well characterized, how cells reprogram the translation 
      machinery for selective gene expression remains poorly understood. Here, we found 
      that the noncanonical 5' cap-binding protein eIF3d was activated in response to 
      metabolic stress in human cells. Activation required reduced CK2-mediated 
      phosphorylation near the eIF3d cap-binding pocket. eIF3d controls a gene program 
      enriched in factors important for glucose homeostasis, including members of the 
      mammalian target of rapamycin (mTOR) pathway. eIF3d-directed translation 
      adaptation was essential for cell survival during chronic glucose deprivation. 
      Thus, this mechanism of translation reprogramming regulates the cellular response 
      to metabolic stress.
CI  - Copyright (c) 2020 The Authors, some rights reserved; exclusive licensee American 
      Association for the Advancement of Science. No claim to original U.S. Government 
      Works.
FAU - Lamper, Adam M
AU  - Lamper AM
AUID- ORCID: 0000-0002-7895-8038
AD  - Department of Biology, Brandeis University, Waltham, MA 02453, USA. 
      amysiyinglee@gmail.com.
FAU - Fleming, Rebecca H
AU  - Fleming RH
AUID- ORCID: 0000-0002-0813-7250
AD  - Department of Biology, Brandeis University, Waltham, MA 02453, USA.
FAU - Ladd, Kayla M
AU  - Ladd KM
AUID- ORCID: 0000-0001-5289-4729
AD  - Department of Biology, Brandeis University, Waltham, MA 02453, USA.
FAU - Lee, Amy S Y
AU  - Lee ASY
AUID- ORCID: 0000-0002-4121-0720
AD  - Department of Biology, Brandeis University, Waltham, MA 02453, USA. 
      amysiyinglee@gmail.com.
LA  - eng
GR  - T32 GM007122/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Science
JT  - Science (New York, N.Y.)
JID - 0404511
RN  - 0 (EIF3D protein, human)
RN  - 0 (Eukaryotic Initiation Factor-3)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
CIN - Mol Cell. 2021 Jan 7;81(1):10-12. PMID: 33417853
MH  - Adaptation, Physiological
MH  - Cell Survival
MH  - Eukaryotic Initiation Factor-3/*biosynthesis/genetics
MH  - Glucose/*deficiency
MH  - HEK293 Cells
MH  - Humans
MH  - Phosphorylation
MH  - *Protein Biosynthesis
MH  - *Stress, Physiological
MH  - TOR Serine-Threonine Kinases/metabolism
EDAT- 2020/11/14 06:00
MHDA- 2020/12/15 06:00
CRDT- 2020/11/13 05:45
PHST- 2020/01/29 00:00 [received]
PHST- 2020/08/20 00:00 [revised]
PHST- 2020/09/24 00:00 [accepted]
PHST- 2020/11/13 05:45 [entrez]
PHST- 2020/11/14 06:00 [pubmed]
PHST- 2020/12/15 06:00 [medline]
AID - 370/6518/853 [pii]
AID - 10.1126/science.abb0993 [doi]
PST - ppublish
SO  - Science. 2020 Nov 13;370(6518):853-856. doi: 10.1126/science.abb0993.