ArticleJournal of cellular physiology2010
TNFAIP8: a new effector for Galpha(i) coupling to reduce cell death and induce cell transformation.
Article in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- The activity level of follicular helper T cells in the peripheral blood of osteosarcoma patients is associated with poor prognosis.Bioengineered · 2022Trial
- TIPE2 suppresses ferroptosis and pro-inflammatory polarization in macrophages triggered by SARS-CoV-2 spike protein.Scientific reports · 2025Article
- TIPE proteins control directed migration of human T cells by directing GPCR and lipid second messenger signaling.Journal of leukocyte biology · 2024Article
- Article
- Dendritic cells transduced with TIPE-2 recombinant adenovirus induces T cells suppression.Journal of inflammation (London, England) · 2021Article
- Expression of TIPE family members in human colorectal cancer.Oncology letters · 2021Article
- Chlorotoxin fusion protein regulates miR-374a and TNFAIP8 expression and inhibits glioma cell proliferation and promotes apoptosis.Cytotechnology · 2020Article
- TNFAIP8: Inflammation, Immunity and Human Diseases.Journal of cellular immunology · 2019Article
- Review
- Structural basis of Gip1 for cytosolic sequestration of G protein in wide-range chemotaxis.Nature communications · 2018Article
- Tumor Necrosis Factor-α Induced Protein 8: Pathophysiology, Clinical Significance, and Regulatory Mechanism.International journal of biological sciences · 2018Review
- Article
- MicroRNA-138 directly targets TNFAIP8 and acts as a tumor suppressor in osteosarcoma.Experimental and therapeutic medicine · 2017Article
- The Tnfaip8-PE complex is a novel upstream effector in the anti-autophagic action of insulin.Scientific reports · 2017Article
- Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins.Cellular & molecular immunology · 2017Review
- 3'-hydroxy-3,4,5,4'-tetramethoxystilbene, the metabolite of resveratrol analogue DMU-212, inhibits ovarian cancer cell growth in vitro and in a mice xenograft model.Scientific reports · 2016Article
- Expression of tumor necrosis factor-α-induced protein 8 in stage III gastric cancer and the correlation with DcR3 and ERK1/2.Oncology letters · 2016Article
- Tumor-suppressive miR-99a inhibits cell proliferation via targeting of TNFAIP8 in osteosarcoma cells.American journal of translational research · 2016Article
- Clinical significance of TIPE expression in gastric carcinoma.OncoTargets and therapy · 2016Article
- Rhodiola rosea suppresses thymus T-lymphocyte apoptosis by downregulating tumor necrosis factor-α-induced protein 8-like-2 in septic rats.International journal of molecular medicine · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Galpha(i)-coupled receptors comprise a diverse family of receptors that induce transformation by largely unknown mechanisms. We previously found that the Galpha(i)-coupled dopamine-D2short (D2S) receptor transforms Balb-D2S cells via Gαi3. To identify new Gαi effectors, a yeast two-hybrid screen was done using constitutively active Gαi3-Q204L as bait, and tumor necrosis factor-alpha (TNFα)-induced protein 8 (TNFAIP8, SCC-S2/NDED/GG2-1) was identified. In contrast, TNFAIP8-related TIPE1 and TIPE2 showed a very weak interaction with Gαi3. In yeast mating, in vitro pull-down, co-immunoprecipitation and bioluminescence resonance energy transfer (BRET) assays, TNFAIP8 preferentially interacted with activated Gαi proteins, consistent with direct Gαi-TNFAIP8 coupling. Over-expression or depletion of TNFAIP8 using antisense constructs in Balb-D2S cells did not affect D2S-induced signaling to Gαi-dependent inhibition of cAMP. In contrast, antisense depletion of TNFAIP8 completely inhibited spontaneous and D2S-induced foci formation, consistent with a role for TNFAIP8 in Gαi-dependent transformation. To address possible mechanisms, the effect of D2S signaling via TNFAIP8 on TNFα action was examined. D2S receptor activation inhibited TNFα-induced cell death in Balb-D2S cells, but not in cells depleted of TNFAIP8. However, depletion of TNFAIP8 did not prevent D2S-induced inhibition of TNFα-mediated caspase activation, suggesting that D2S/TNFAIP8-induced protection from TNFα-induced cell death is caspase-independent. The data suggest that Gαi-TNFAIP8-mediated rescue of pre-oncogenic cells enhances progression to oncogenic transformation, providing a selective target to inhibit cellular transformation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.