ArticleMolecular biology of the cell2013
Drosophila SOCS36E negatively regulates JAK/STAT pathway signaling via two separable mechanisms.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Article
- A regulatory loop of JAK/STAT signalling and its downstream targets represses cell fate conversion and maintains male germline stem cell niche homeostasis.Cell proliferation · 2024Article
- Fat- and sugar-induced signals regulate sweet and fat taste perception in Drosophila.Cell reports · 2023Article
- A global genetic interaction network by single-cell imaging and machine learning.Cell systems · 2023Article
- Mutual repression between JNK/AP-1 and JAK/STAT stratifies senescent and proliferative cell behaviors during tissue regeneration.PLoS biology · 2023Article
- Germline protein, Cup, non-cell autonomously limits migratory cell fate in Drosophila oogenesis.PLoS genetics · 2023Article
- The Intestinal Immune Defense System in Insects.International journal of molecular sciences · 2022Review
- Review
- Coordination of tumor growth and host wasting by tumor-derived Upd3.Cell reports · 2021Article
- Thymoquinone Suppresses Cell Proliferation and Enhances Apoptosis of HL60 Leukemia Cells through Re-Expression of JAK/STAT Negative Regulators.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Proteasome α6 Subunit Negatively Regulates the JAK/STAT Pathway and Blood Cell Activation inFrontiers in immunology · 2021Article
- Rounding up the Usual Suspects: Assessing Yorkie, AP-1, and Stat Coactivation in Tumorigenesis.International journal of molecular sciences · 2020Article
- A genome-wide RNAi screen identifies MASK as a positive regulator of cytokine receptor stability.Journal of cell science · 2018Article
- Re-Expression of Bone Marrow Proteoglycan-2 by 5-Azacytidine is associated with STAT3 Inactivation and Sensitivity Response to Imatinib in Resistant CML CellsAsian Pacific journal of cancer prevention : APJCP · 2018Article
- Article
- Age and Diet Affect Genetically Separable Secondary Injuries that Cause Acute Mortality Following Traumatic Brain Injury in Drosophila.G3 (Bethesda, Md.) · 2016Article
- β-Arrestin 1's Interaction with TC45 Attenuates Stat signaling by dephosphorylating Stat to inhibit antimicrobial peptide expression.Scientific reports · 2016Article
- Remote Control of Intestinal Stem Cell Activity by Haemocytes in Drosophila.PLoS genetics · 2016Article
- Apontic regulates somatic stem cell numbers in Drosophila testes.BMC developmental biology · 2016Article
- Mechanisms of JAK/STAT pathway negative regulation by the short coreceptor Eye Transformer/Latran.Molecular biology of the cell · 2016Article
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Abstract
Conserved from humans to Drosophila, the Janus kinase/signal transducer and activators of transcription (JAK/STAT) signaling cascade is essential for multiple developmental and homeostatic processes, with regulatory molecules controlling pathway activity also highly conserved. We characterize the Drosophila JAK/STAT pathway regulator SOCS36E and show that it functions via two independent mechanisms. First, we show that Drosophila Elongin B/C and Cullin-5 act via the SOCS-box of SOCS36E to reduce pathway activity specifically in response to ligand stimulation--a process that involves endocytic trafficking and lysosomal degradation of the Domeless (Dome) receptor. Second, SOCS36E also suppresses both stimulated and basal pathway activity via an Elongin/Cullin-independent mechanism that is mediated by the N-terminus of SOCS36E, which is required for the physical interaction of SOCS36E with Dome. Although some human SOCS proteins contain N-terminal kinase-inhibitory domains, we do not identify such a region in SOCS36E and propose a model wherein the N-terminal of SOCS36E blocks access to tyrosine residues in Dome. Our biochemical analysis of a SOCS-family regulator from a lower organism highlights the fundamental conserved roles played by regulatory mechanisms in signal transduction.
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