TNFAIP8L3

Last update 08 May 2025

Basic Info

Synonyms

FLJ41287, TIPE3, TNF alpha induced protein 8 like 3

+ [4]

Introduction

Acts as a lipid transfer protein. Preferentially captures and shuttles two lipid second messengers, i.e., phosphatidylinositol 4,5- bisphosphate and phosphatidylinositol 3,4,5-trisphosphate and increases their levels in the plasma membrane. Additionally, may also function as a lipid-presenting protein to enhance the activity of the PI3K-AKT and MEK-ERK pathways. May act as a regulator of tumorigenesis through its activation of phospholipid signaling.

100 Clinical Results associated with TNFAIP8L3

100 Translational Medicine associated with TNFAIP8L3

0 Patents (Medical) associated with TNFAIP8L3

Literatures (Medical) associated with TNFAIP8L3

28 Oct 2024·Journal of Clinical and Experimental Hematopathology

Transcriptome analysis of the cytokine storm-related genes among the subtypes of idiopathic multicentric Castleman disease

Article

Author: Chijimatsu, Ryota ; Ochi, Sayaka ; Sato, Yasuharu ; Takeda, Yudai ; Kawahara, Yuri ; Nishimura, Midori Filiz ; Tomida, Shuta ; Nakamura, Naoya ; Ennishi, Daisuke ; Haratake, Tomoka ; Momose, Shuji ; Ueta, Himawari ; Lai, You Cheng ; Nishikori, Asami

Idiopathic multicentric Castleman disease (iMCD) is a type of Castleman disease unrelated to the Kaposi sarcoma-associated herpesvirus/human herpesvirus type 8 (KSHV/HHV8) infection. Presently, iMCD is classified into iMCD-IPL (idiopathic plasmacytic lymphadenopathy), iMCD-TAFRO (thrombocytopenia, anasarca, fever, reticulin fibrosis/renal insufficiency, and organomegaly), and iMCD-NOS (not otherwise specified). The most common treatment for iMCD is using IL-6 inhibitors; however, some patients resist IL-6 inhibitors, especially for iMCD-TAFRO/NOS. Nevertheless, since serum IL-6 levels are not significantly different between the iMCD-IPL and iMCD-TAFRO/NOS cases, cytokines other than IL-6 may be responsible for the differences in pathogenesis. Herein, we performed a transcriptome analysis of cytokine storm-related genes and examined the differences between iMCD-IPL and iMCD-TAFRO/NOS. The results demonstrated that counts per million of STAT2, IL1R1, IL1RAP, IL33, TAFAIP1, and VEGFA (P < 0.001); STAT3, JAK2, MAPK8, IL17RA, IL18, TAFAIP2, TAFAIP3, PDGFA, VEGFC, CXCL10, CCL4, and CXCL13 (P < 0.01); and STAT1, STAT6, JAK1, MAPK1, MAPK3, MAPK6, MAPK7, MAPK9, MAPK10, MAPK11, MAPK12, MAPK14, NFKB1, NFKBIA, NFKBIB, NFKBIZ, MTOR, IL10RB, IL12RB2, IL18BP, TAFAIP6, TNFAIP8L1, TNFAIP8L3, CSF2RBP1, PDGFB, PDGFC, and CXCL9 (P < 0.05) were significantly increased in iMCD-TAFRO/NOS. Particularly, upregulated IL33 expression was demonstrated for the first time in iMCD-TAFRO/NOS. Thus, inflammatory signaling, such as JAK-STAT and MAPK, may be enhanced in iMCD-TAFRO/NOS and may be a cytokine storm.

01 Jun 2024·Experimental Cell Research

Down-regulated expression of TIPE3 inhibits malignant progression of non-small cell lung cancer via Wnt signaling

Article

Author: Zong, Zhenfeng ; Tang, Guojie ; Guo, Yu ; Kong, Fanyi

Non-small cell lung cancer (NSCLC) accounts for approximately 80 % of all lung cancers with a low five-year survival rate. Therefore, the mechanistic pathways and biomarkers of NSCLC must be explored to elucidate its pathogenesis. In this study, we examined TIPE3 expression in NSCLC cells and investigated the molecular mechanisms underlying NSCLC regulation in vivo and in vitro. We collected tissue samples from patients with NSCLC to examine TIPE3 expression and its association with patient metastasis and prognosis. Furthermore, we evaluated the expression level of TIPE3 in NSCLC cells. Cell lines with the highest expression were selected for molecular mechanism experiments, and animal models were established for in vivo verification. The results showed that TIPE3 was significantly increased in patients with NSCLC, and this increased expression was associated with tumor metastasis and patient prognosis. TIPE3 knockdown inhibited proliferation, migration, invasion, EMT, angiogenesis, and tumorsphere formation in NSCLC cells. Moreover, it reduced the metabolic levels of tumor cells. However, overexpression of TIPE3 has the opposite effect. The in vivo results showed that TIPE3 knockdown reduced tumor volume, weight, and metastasis. Furthermore, the results showed that TIPE3 may inhibit malignant progression of NSCLC via the regulation of Wnt/β-catenin expression. These findings suggest that TIPE3 is significantly elevated in patients with NSCLC and that downregulation of TIPE3 can suppress the malignant progression of NSCLC, which could serve as a potential diagnostic and treatment strategy for NSCLC.

01 Mar 2024·Asian Journal of Surgery

Comprehensive analysis of the prognostic and immunological roles of TIPE3 in Colon Cancer

Letter

Author: Xu, A-Man ; Zhu, Xiao-Dong ; Zhu, Yong ; Xia, Heng-Bo

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TNFAIP8L3

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