MAPK8IP2

Last update 08 May 2025

Basic Info

Synonyms

C-Jun-amino-terminal kinase-interacting protein 2, IB-2, IB2

+ [9]

Introduction

The JNK-interacting protein (JIP) group of scaffold proteins selectively mediates JNK signaling by aggregating specific components of the MAPK cascade to form a functional JNK signaling module. JIP2 inhibits IL1 beta-induced apoptosis in insulin-secreting cells. May function as a regulator of vesicle transport, through interactions with the JNK-signaling components and motor proteins (By similarity).

100 Clinical Results associated with MAPK8IP2

100 Translational Medicine associated with MAPK8IP2

0 Patents (Medical) associated with MAPK8IP2

Literatures (Medical) associated with MAPK8IP2

01 Apr 2025·International Journal of Biological Macromolecules

Selection of biofilm-inhibiting ssDNA aptamers against antibiotic-resistant Edwardsiella tarda by inhibition-SELEX and interaction with their binding proteins

Article

Author: Yan, Qingpi ; Huang, Lixing ; Wang, Jiaen ; Fan, Yunting ; Tan, Ying ; Weng, Qibiao ; Zheng, Jiang

Biofilms can increase bacterial resistance to antibiotic therapies. Edwardsiella tarda with biofilm is highly resistant to antibacterial treatment, especially for the antibiotic-resistant strain. In this study, we obtained biofilm-inhibiting aptamers against antibiotic-resistant E. tarda via a novel systematic evolution of ligands by exponential enrichment (SELEX) technique, called inhibition-SELEX. After four rounds of screening and validation, we identified aptamers IB1, IB2, and IB3, which demonstrated biofilm-inhibition and biofilm-degradation rates of 69 %, 75 %, and 62 % and 51 %, 63 %, and 45 % at 2 μmol/L, respectively, against antibiotic-resistant E. tarda. Magnetic separation, SDS-PAGE, and mass spectrometry analyses revealed that all three aptamers could bind to glyceraldehyde-3-phosphate dehydrogenase (GAPDH), while IB2 could also bind to formate C-acetyltransferase (FA). Through molecular docking and molecular dynamics simulations, it was found that the four complexes primarily interact through hydrogen bonding. Among them, IB1-GAPDH exhibited the strongest stability, followed by IB2-FA, then IB2-GAPDH, and IB3-GAPDH was the least stable. Our results suggest that IB1, IB2, and IB3 may inhibit and degrade E. tarda biofilm by interfering with the synthesis, secretion, and transportation of its extracellular polysaccharides and proteins by interacting with GAPDH and FA.

01 Jan 2025·[Rinsho ketsueki] The Japanese journal of clinical hematology

[Comparison of IPSS-R and IPSS-M in newly diagnosed myelodysplastic neoplasms: a single-center study].

Article

Author: Akahane, Daigo ; Harada, Hironori ; Yamada, Akiko ; Gotoh, Moritaka ; Furuya, Nahoko ; Moriyama, Mituru ; Harada, Yuka ; Fujimoto, Hiroaki ; Katagiri, Seiichiro ; Otsuki, Shunsuke ; Okabe, Seiichi ; Gotoh, Akihiko ; Suguro, Tamiko ; Ito, Yoshikazu ; Wakamatsu, Shohei ; Tanaka, Yuko ; Yoshizawa, Seiichiro ; Asano, Michiyo ; Arai, Yuya

We compared the International Prognostic Scoring System-Revised (IPSS-R) to the International Prognostic Scoring System-Molecular (IPSS-M) in 30 patients with myelodysplastic neoplasms (MDS) newly diagnosed at our institution from January 2021 to February 2023. Molecular analysis was performed by myeloid panel. The median age was 66 years (range: 35-80), and classifications were MDS-LB (n=18), MDS IB-1 (n=1), MDS IB-2 (n=2), MDS-SF3B1 (n=2), MDS-biTP53 (n=1), and MN-pCT (n=6). Each patient had 0 to 8 (median 1) mutations. The most frequently detected mutation was the TET2 mutation, and others detected in>5 patients were U2AF1, TP53, and RUNX1 mutations. IPSS-R classification indicated that 2, 14, 5, 3, and 6 patients were very low, low, intermediate (Int), high, and very high risk, respectively, whereas the IPSS-M classification indicated that 3, 9, 7, 2, 4, and 5 cases were very low, low, moderate-low (ML), moderate-high (MH), high, and very high risk, respectively. Considering IPSS-M ML and MH as the equivalent to IPSS-R Int, 13 (43%) patients had a different risk level in the IPSS-M compared to the IPSS-R. One patient was rated low-risk by IPSS-R, but reclassified as high risk by IPSS-M. It is important to be mindful of this potential for significant discrepancies between risk assessments using IPSS-R and IPSS-M in some cases when making treatment decisions.

01 Dec 2024·International Immunopharmacology

SLAMF1 as a novel molecule mediating the causal association between rheumatoid arthritis and interstitial lung disease: A Mendelian randomization study combined with transcriptomics and in vivo validation

Article

Author: Liu, Muqiu ; Li, Yanwu ; Du, Qun ; Jiang, Zhihao ; Liu, Min ; Dong, Yan ; Fang, Jiansong ; Ni, Haojie

BACKGROUNDRheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a common complication of rheumatoid arthritis (RA) that result in significant morbidity and mortality. Understanding the molecular mechanisms underlying RA-ILD is crucial for effective prevention. This study aims to identify the specific molecule that mediate the causal association between RA and ILD, as well as to explore its potential mechanisms in the pathogenesis of RA-ILD.METHODSUsing two-sample Mendelian randomization (MR) analyses, we investigated the causal relationship among 16,987 blood genes, RA and ILD. Subsequently, a two-step MR technique was employed to identify significant genes that mediate the association between RA and ILD, and to quantify their proportion of mediation effect. To validate the genes as mediators, the replication MR analysis was conducted and the in vivo experiment was performed using an established animal model of RA-ILD. Furthermore, integrated bioinformatic analyses were conducted to elucidate the specific biological functions of the determined mediator in pathogenesis of RA-ILD.RESULTSNine genes, namely MAPK8IP2, TAF11, SLAMF1, DAB2IP, GLUL, SLC4A10, PRSS35, NFX1, and PLK3, were identified as mediators. Among them, SLAMF1 was validated as the most significant mediator, accounting for 4.693% of the mediating effect on the causal relationship between RA and ILD. Upregulated mRNA expression of SLAMF1 was observed in the animal model of RA-ILD compared to controls. Bioinformatic analyses revealed that SLAMF1 was overexpressed in patients with lung fibrosis and correlated with a poor prognosis. Specifically, SLAMF1 was found to be predominantly overexpressed in T cells in lung tissues of patients with lung fibrosis. Additionally, the functional role of SLAMF1 was associated with multiple immune cell infiltrations and the biological process of extracellular matrix synthesis in pulmonary tissues from patients with lung fibrosis.CONCLUSIONSLAMF1 may play a crucial role as a molecular mediator in the causal association between RA and ILD, and participate in multiple mechanisms underlying the pathogenesis of RA-ILD. This research provides insights into how the development of RA influences the risk of ILD and offers potential interventional targets against RA-ILD.

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MAPK8IP2

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