mTORC1 promotes cell growth via m

Adenosine / analogs & derivatives Animals Base Sequence Cell Cycle Proteins / metabolism Cell Line, Tumor Cell Proliferation Eukaryotic Initiation Factors / metabolism HEK293 Cells Humans Male Mechanistic Target of Rapamycin Complex 1 / metabolism Mice Models, Biological Protein Biosynthesis Proto-Oncogene Proteins c-myc / metabolism RNA Splicing Factors / metabolism RNA Stability RNA, Messenger / genetics Ribosomal Protein S6 Kinases / metabolism Signal Transduction
MXD2 Protein translation S6K1 WTAP YTHDF readers cMyc eIF4A m(6)A mRNA modification mRNA stability mTORC1

Journal

Molecular cell
ISSN: 1097-4164
Titre abrégé: Mol Cell
Pays: United States
ID NLM: 9802571

Informations de publication

Date de publication:
20 05 2021
Historique:
received: 31 07 2020
revised: 21 01 2021
accepted: 08 03 2021
pubmed: 24 3 2021
medline: 17 6 2021
entrez: 23 3 2021
Statut: ppublish

Résumé

Dysregulated mTORC1 signaling alters a wide range of cellular processes, contributing to metabolic disorders and cancer. Defining the molecular details of downstream effectors is thus critical for uncovering selective therapeutic targets. We report that mTORC1 and its downstream kinase S6K enhance eIF4A/4B-mediated translation of Wilms' tumor 1-associated protein (WTAP), an adaptor for the N

Identifiants

DOI: 10.1016/j.molcel.2021.03.010 PMID: 33756105 PMC: PMC8356906
pubmed: 33756105
pii: S1097-2765(21)00178-7
doi: 10.1016/j.molcel.2021.03.010
pmc: PMC8356906
mid: NIHMS1705823
pii:
doi:

Substances chimiques

Cell Cycle Proteins 0
Eukaryotic Initiation Factors 0
Proto-Oncogene Proteins c-myc 0
RNA Splicing Factors 0
RNA, Messenger 0
WTAP protein, human 0
eIF-4B 0
N-methyladenosine CLE6G00625
Mechanistic Target of Rapamycin Complex 1 EC 2.7.11.1
Ribosomal Protein S6 Kinases EC 2.7.11.1
Adenosine K72T3FS567

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2064-2075.e8

Subventions

Organisme : NIH HHS
ID : S10 OD023669
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL121266
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA062948
Pays : United States
Organisme : NIDDK NIH HHS
ID : DP1 DK113643
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA203702
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA120964
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR057352
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM051405
Pays : United States
Organisme : NCI NIH HHS
ID : F32 CA221104
Pays : United States
Organisme : NINDS NIH HHS
ID : R35 NS111631
Pays : United States
Organisme : Howard Hughes Medical Institute
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA186702
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests J.B. is an advisory board member for Molecular Cell. S.R.J. is scientific founder of, is advisor to, and owns equity in Gotham Therapeutics.

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Auteurs

Sungyun Cho (S)

Department of Pharmacology, Meyer Cancer Center, Weill Cornell Medicine, Cornell University, New York, NY, USA.

Gina Lee (G)

Department of Pharmacology, Meyer Cancer Center, Weill Cornell Medicine, Cornell University, New York, NY, USA; Department of Microbiology and Molecular Genetics, Chao Family Comprehensive Cancer Center, University of California Irvine School of Medicine, Irvine, CA, USA. Electronic address: ginalee@uci.edu.

Brian F Pickering (BF)

Department of Pharmacology, Meyer Cancer Center, Weill Cornell Medicine, Cornell University, New York, NY, USA.

Cholsoon Jang (C)

Department of Chemistry, Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ, USA; Department of Biological Chemistry, Chao Family Comprehensive Cancer Center, University of California Irvine School of Medicine, Irvine, CA, USA.

Jin H Park (JH)

Department of Pharmacology, Meyer Cancer Center, Weill Cornell Medicine, Cornell University, New York, NY, USA.

Long He (L)

Department of Pharmacology, Meyer Cancer Center, Weill Cornell Medicine, Cornell University, New York, NY, USA.

Lavina Mathur (L)

Department of Microbiology and Molecular Genetics, Chao Family Comprehensive Cancer Center, University of California Irvine School of Medicine, Irvine, CA, USA.

Seung-Soo Kim (SS)

Department of Obstetrics and Gynecology, Irving Medical Center, Columbia University, New York, NY, USA.

Sunhee Jung (S)

Department of Biological Chemistry, Chao Family Comprehensive Cancer Center, University of California Irvine School of Medicine, Irvine, CA, USA.

Hong-Wen Tang (HW)

Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA; Program in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore, Singapore.

Sebastien Monette (S)

Laboratory of Comparative Pathology, Memorial Sloan Kettering Cancer Center, The Rockefeller University, Weill Cornell Medicine, New York, NY, USA.

Joshua D Rabinowitz (JD)

Department of Chemistry, Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ, USA.

Norbert Perrimon (N)

Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA; Howard Hughes Medical Institute, Boston, MA, USA.

Samie R Jaffrey (SR)

Department of Pharmacology, Meyer Cancer Center, Weill Cornell Medicine, Cornell University, New York, NY, USA. Electronic address: srj2003@med.cornell.edu.

John Blenis (J)

Department of Pharmacology, Meyer Cancer Center, Weill Cornell Medicine, Cornell University, New York, NY, USA. Electronic address: job2064@med.cornell.edu.

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Classifications MeSH

questionsmedicales.fr › Acides nucléiques, nucléotides et nucléosides › Nucléosides › Ribonucléosides › Adénosine › mTORC1 promotes cell growth via m
questionsmedicales.fr › Eucaryotes › Animaux › mTORC1 promotes cell growth via m
questionsmedicales.fr › Sciences de l'information › Sources d'information › Services d'information › Documentation › Données de séquences moléculaires › Séquence nucléotidique › mTORC1 promotes cell growth via m
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines du cycle cellulaire › mTORC1 promotes cell growth via m
questionsmedicales.fr › Cellules › Cellules cultivées › Cellules cancéreuses en culture › Lignée cellulaire tumorale › mTORC1 promotes cell growth via m
questionsmedicales.fr › Phénomènes physiologiques › Croissance et développement › Croissance › Processus de croissance cellulaire › Prolifération cellulaire › mTORC1 promotes cell growth via m
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines ribosomiques › Facteurs initiation chaîne peptidique › Facteurs d'initiation eucaryotes › mTORC1 promotes cell growth via m
questionsmedicales.fr › Cellules › Cellules épithéliales › Cellules HEK293 › mTORC1 promotes cell growth via m
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › mTORC1 promotes cell growth via m
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines et peptides de signalisation intracellulaire › Protein-Serine-Threonine Kinases › Sérine-thréonine kinases TOR › Complexe-1 cible mécanistique de la rapamycine › mTORC1 promotes cell growth via m
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › mTORC1 promotes cell growth via m
questionsmedicales.fr › Techniques d'investigation › Modèles théoriques › Modèles biologiques › mTORC1 promotes cell growth via m
questionsmedicales.fr › Phénomènes génétiques › Expression des gènes › Biosynthèse des protéines › mTORC1 promotes cell growth via m
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Facteurs de transcription › Facteurs de transcription à motif basique hélice-boucle-hélice › Protéines proto-oncogènes c-myc › mTORC1 promotes cell growth via m
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Nucléoprotéines › Protéines de liaison à l'ARN › Facteurs d'épissage des ARN › mTORC1 promotes cell growth via m
questionsmedicales.fr › Phénomènes chimiques › Phénomènes biochimiques › Stabilité de l'ARN › mTORC1 promotes cell growth via m
questionsmedicales.fr › Acides nucléiques, nucléotides et nucléosides › Acides nucléiques › ARN › ARN messager › mTORC1 promotes cell growth via m
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines et peptides de signalisation intracellulaire › Protein-Serine-Threonine Kinases › Ribosomal Protein S6 Kinases › mTORC1 promotes cell growth via m
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Transduction du signal › mTORC1 promotes cell growth via m