期刊
NEURON
卷 73, 期 2, 页码 374-390出版社
CELL PRESS
DOI: 10.1016/j.neuron.2011.11.024
关键词
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资金
- MRC
- BBSRC
- Inserm
- Universite Paris Diderot
- PremUP
- Fondation Roger de Spoelberch
- Fondation Grace de Monaco
- Leducq Foundation
- WCU through the KOSEF
- MEST [R31-10089]
- Korean Ministry of Science and Technology
- BK21 fellowship
- Universite Denis Diderot-Paris 7
- Assistance publique-Hopitaux de Paris (AP-HP) (Contrat d'Interface)
- Association pour la Recherche sur le Cancer (ARC)
- Federation pour la Recherche sur le Cerveau (FRC)
- BBSRC [BB/G003963/1, BB/H006451/1] Funding Source: UKRI
- MRC [MC_G1000734, G0601813] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/H006451/1, BB/G003963/1] Funding Source: researchfish
- Medical Research Council [G0601841B, MC_G1000734, G0601813] Funding Source: researchfish
The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is involved in many cellular processes, including cell growth and differentiation, immune functions and cancer. It is activated by various cytokines, growth factors, and protein tyrosine kinases (PTKs) and regulates the transcription of many genes. Of the four JAK isoforms and seven STAT isoforms known, JAK2 and STAT3 are highly expressed in the brain where they are present in the postsynaptic density (PSD). Here, we demonstrate a new neuronal function for the JAK/STAT pathway. Using a variety of complementary approaches, we show that the JAK/STAT pathway plays an essential role in the induction of NMDA-receptor dependent long-term depression (NMDAR-LTD) in the hippocampus. Therefore, in addition to established roles in cytokine signaling, the JAK/STAT pathway is involved in synaptic plasticity in the brain.
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