RapamycinFungusV1, Main, Exploration, bibRecord, 000B23

Cutting Edge: Foxp1 Controls Naive CD8+ T Cell Quiescence by Simultaneously Repressing Key Pathways in Cellular Metabolism and Cell Cycle Progression.

Identifieur interne : 000B23 ( Main/Exploration ); précédent : 000B22; suivant : 000B24

Cutting Edge: Foxp1 Controls Naive CD8+ T Cell Quiescence by Simultaneously Repressing Key Pathways in Cellular Metabolism and Cell Cycle Progression.

Auteurs : Hairong Wei [États-Unis] ; Jianlin Geng [États-Unis] ; Bi Shi [États-Unis] ; Zhenghui Liu [États-Unis] ; Yin-Hu Wang [États-Unis] ; Anna C. Stevens [États-Unis] ; Stephanie L. Sprout [États-Unis] ; Min Yao [République populaire de Chine] ; Haikun Wang [République populaire de Chine] ; Hui Hu [République populaire de Chine]

Source :

Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2016.

RBID : pubmed:27001958

Descripteurs français

KwdFr :
- Animaux (MeSH), Cycle cellulaire (physiologie), Facteurs de transcription Forkhead (déficit), Facteurs de transcription Forkhead (génétique), Facteurs de transcription Forkhead (métabolisme), Homéostasie (MeSH), Interleukine-7 (immunologie), Interleukine-7 (métabolisme), Interleukine-7 (pharmacologie), Lymphocytes T CD8+ (cytologie), Lymphocytes T CD8+ (effets des médicaments et des substances chimiques), Lymphocytes T CD8+ (immunologie), Lymphocytes T CD8+ (métabolisme), Phosphatidylinositol 3-kinases (génétique), Phosphatidylinositol 3-kinases (métabolisme), Phosphorylation (MeSH), Prolifération cellulaire (MeSH), Protéine du rétinoblastome (immunologie), Protéine du rétinoblastome (métabolisme), Protéines de répression (déficit), Protéines de répression (génétique), Protéines de répression (métabolisme), Protéines de transport (génétique), Protéines de transport (métabolisme), Régulation de l'expression des gènes (MeSH), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH).
MESH :
- cytologie : Lymphocytes T CD8+.
- déficit : Facteurs de transcription Forkhead, Protéines de répression.
- effets des médicaments et des substances chimiques : Lymphocytes T CD8+.
- génétique : Facteurs de transcription Forkhead, Phosphatidylinositol 3-kinases, Protéines de répression, Protéines de transport.
- immunologie : Interleukine-7, Lymphocytes T CD8+, Protéine du rétinoblastome.
- métabolisme : Facteurs de transcription Forkhead, Interleukine-7, Lymphocytes T CD8+, Phosphatidylinositol 3-kinases, Protéine du rétinoblastome, Protéines de répression, Protéines de transport, Sérine-thréonine kinases TOR.
- pharmacologie : Interleukine-7.
- physiologie : Cycle cellulaire.
- Animaux, Homéostasie, Phosphorylation, Prolifération cellulaire, Régulation de l'expression des gènes, Transduction du signal.

English descriptors

KwdEn :
- Animals (MeSH), CD8-Positive T-Lymphocytes (cytology), CD8-Positive T-Lymphocytes (drug effects), CD8-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (metabolism), Carrier Proteins (genetics), Carrier Proteins (metabolism), Cell Cycle (physiology), Cell Proliferation (MeSH), Forkhead Transcription Factors (deficiency), Forkhead Transcription Factors (genetics), Forkhead Transcription Factors (metabolism), Gene Expression Regulation (MeSH), Homeostasis (MeSH), Interleukin-7 (immunology), Interleukin-7 (metabolism), Interleukin-7 (pharmacology), Phosphatidylinositol 3-Kinases (genetics), Phosphatidylinositol 3-Kinases (metabolism), Phosphorylation (MeSH), Repressor Proteins (deficiency), Repressor Proteins (genetics), Repressor Proteins (metabolism), Retinoblastoma Protein (immunology), Retinoblastoma Protein (metabolism), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (metabolism).
MESH :
- chemical , deficiency : Forkhead Transcription Factors, Repressor Proteins.
- chemical , genetics : Carrier Proteins, Forkhead Transcription Factors, Phosphatidylinositol 3-Kinases, Repressor Proteins.
- cytology : CD8-Positive T-Lymphocytes.
- drug effects : CD8-Positive T-Lymphocytes.
- immunology : CD8-Positive T-Lymphocytes, Interleukin-7, Retinoblastoma Protein.
- metabolism : CD8-Positive T-Lymphocytes, Carrier Proteins, Forkhead Transcription Factors, Interleukin-7, Phosphatidylinositol 3-Kinases, Repressor Proteins, Retinoblastoma Protein, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Interleukin-7.
- physiology : Cell Cycle.
- Animals, Cell Proliferation, Gene Expression Regulation, Homeostasis, Phosphorylation, Signal Transduction.

Abstract

Previously we have shown that transcription factor Foxp1 plays an essential role in maintaining naive T cell quiescence; in the absence of Foxp1, mature naive CD8(+) T cells proliferate in direct response to homeostatic cytokine IL-7. In this study, we report that the deletion of Foxp1 in naive CD8(+) T cells leads to enhanced activation of the PI3K/Akt/mammalian target of rapamycin signaling pathway and its downstream cell growth and metabolism targets in response to IL-7. We found that Foxp1 directly regulates PI3K interacting protein 1, a negative regulator of PI3K. Additionally, we found that deletion of Foxp1 in naive CD8(+) T cells results in increased expression levels of E2fs, the critical components for cell cycle progression and proliferation, in a manner that is not associated with increased phosphorylation of retinoblastoma protein. Taken together, our studies suggest that Foxp1 enforces naive CD8(+) T cell quiescence by simultaneously repressing key pathways in both cellular metabolism and cell cycle progression.

DOI: 10.4049/jimmunol.1501896
PubMed: 27001958
PubMed Central: PMC4868629

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000A78
to stream Main, to step Curation: 000A78

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>CD8-Positive T-Lymphocytes (cytology)</term>
<term>CD8-Positive T-Lymphocytes (drug effects)</term>
<term>CD8-Positive T-Lymphocytes (immunology)</term>
<term>CD8-Positive T-Lymphocytes (metabolism)</term>
<term>Carrier Proteins (genetics)</term>
<term>Carrier Proteins (metabolism)</term>
<term>Cell Cycle (physiology)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Forkhead Transcription Factors (deficiency)</term>
<term>Forkhead Transcription Factors (genetics)</term>
<term>Forkhead Transcription Factors (metabolism)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Homeostasis (MeSH)</term>
<term>Interleukin-7 (immunology)</term>
<term>Interleukin-7 (metabolism)</term>
<term>Interleukin-7 (pharmacology)</term>
<term>Phosphatidylinositol 3-Kinases (genetics)</term>
<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Phosphorylation (MeSH)</term>
<term>Repressor Proteins (deficiency)</term>
<term>Repressor Proteins (genetics)</term>
<term>Repressor Proteins (metabolism)</term>
<term>Retinoblastoma Protein (immunology)</term>
<term>Retinoblastoma Protein (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Cycle cellulaire (physiologie)</term>
<term>Facteurs de transcription Forkhead (déficit)</term>
<term>Facteurs de transcription Forkhead (génétique)</term>
<term>Facteurs de transcription Forkhead (métabolisme)</term>
<term>Homéostasie (MeSH)</term>
<term>Interleukine-7 (immunologie)</term>
<term>Interleukine-7 (métabolisme)</term>
<term>Interleukine-7 (pharmacologie)</term>
<term>Lymphocytes T CD8+ (cytologie)</term>
<term>Lymphocytes T CD8+ (effets des médicaments et des substances chimiques)</term>
<term>Lymphocytes T CD8+ (immunologie)</term>
<term>Lymphocytes T CD8+ (métabolisme)</term>
<term>Phosphatidylinositol 3-kinases (génétique)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Phosphorylation (MeSH)</term>
<term>Prolifération cellulaire (MeSH)</term>
<term>Protéine du rétinoblastome (immunologie)</term>
<term>Protéine du rétinoblastome (métabolisme)</term>
<term>Protéines de répression (déficit)</term>
<term>Protéines de répression (génétique)</term>
<term>Protéines de répression (métabolisme)</term>
<term>Protéines de transport (génétique)</term>
<term>Protéines de transport (métabolisme)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transduction du signal (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Forkhead Transcription Factors</term>
<term>Repressor Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Carrier Proteins</term>
<term>Forkhead Transcription Factors</term>
<term>Phosphatidylinositol 3-Kinases</term>
<term>Repressor Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Lymphocytes T CD8+</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Facteurs de transcription Forkhead</term>
<term>Protéines de répression</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Lymphocytes T CD8+</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteurs de transcription Forkhead</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines de répression</term>
<term>Protéines de transport</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Interleukine-7</term>
<term>Lymphocytes T CD8+</term>
<term>Protéine du rétinoblastome</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term>
<term>Interleukin-7</term>
<term>Retinoblastoma Protein</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term>
<term>Carrier Proteins</term>
<term>Forkhead Transcription Factors</term>
<term>Interleukin-7</term>
<term>Phosphatidylinositol 3-Kinases</term>
<term>Repressor Proteins</term>
<term>Retinoblastoma Protein</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription Forkhead</term>
<term>Interleukine-7</term>
<term>Lymphocytes T CD8+</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéine du rétinoblastome</term>
<term>Protéines de répression</term>
<term>Protéines de transport</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Interleukine-7</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Interleukin-7</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cycle cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Cycle</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Proliferation</term>
<term>Gene Expression Regulation</term>
<term>Homeostasis</term>
<term>Phosphorylation</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Homéostasie</term>
<term>Phosphorylation</term>
<term>Prolifération cellulaire</term>
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<front><div type="abstract" xml:lang="en">Previously we have shown that transcription factor Foxp1 plays an essential role in maintaining naive T cell quiescence; in the absence of Foxp1, mature naive CD8(+) T cells proliferate in direct response to homeostatic cytokine IL-7. In this study, we report that the deletion of Foxp1 in naive CD8(+) T cells leads to enhanced activation of the PI3K/Akt/mammalian target of rapamycin signaling pathway and its downstream cell growth and metabolism targets in response to IL-7. We found that Foxp1 directly regulates PI3K interacting protein 1, a negative regulator of PI3K. Additionally, we found that deletion of Foxp1 in naive CD8(+) T cells results in increased expression levels of E2fs, the critical components for cell cycle progression and proliferation, in a manner that is not associated with increased phosphorylation of retinoblastoma protein. Taken together, our studies suggest that Foxp1 enforces naive CD8(+) T cell quiescence by simultaneously repressing key pathways in both cellular metabolism and cell cycle progression.</div>
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<Abstract><AbstractText>Previously we have shown that transcription factor Foxp1 plays an essential role in maintaining naive T cell quiescence; in the absence of Foxp1, mature naive CD8(+) T cells proliferate in direct response to homeostatic cytokine IL-7. In this study, we report that the deletion of Foxp1 in naive CD8(+) T cells leads to enhanced activation of the PI3K/Akt/mammalian target of rapamycin signaling pathway and its downstream cell growth and metabolism targets in response to IL-7. We found that Foxp1 directly regulates PI3K interacting protein 1, a negative regulator of PI3K. Additionally, we found that deletion of Foxp1 in naive CD8(+) T cells results in increased expression levels of E2fs, the critical components for cell cycle progression and proliferation, in a manner that is not associated with increased phosphorylation of retinoblastoma protein. Taken together, our studies suggest that Foxp1 enforces naive CD8(+) T cell quiescence by simultaneously repressing key pathways in both cellular metabolism and cell cycle progression.</AbstractText>
<CopyrightInformation>Copyright © 2016 by The American Association of Immunologists, Inc.</CopyrightInformation>
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Cutting Edge: Foxp1 Controls Naive CD8+ T Cell Quiescence by Simultaneously Repressing Key Pathways in Cellular Metabolism and Cell Cycle Progression.

Cutting Edge: Foxp1 Controls Naive CD8+ T Cell Quiescence by Simultaneously Repressing Key Pathways in Cellular Metabolism and Cell Cycle Progression.

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