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Last update 23 Jan 2025

ITGB8

Last update 23 Jan 2025

Basic Info

Synonyms

Integrin beta-8, integrin subunit beta 8, integrin, beta 8

+ [1]

Introduction

Integrin alpha-V:beta-8 (ITGAV:ITGB8) is a receptor for fibronectin (PubMed:1918072). It recognizes the sequence R-G-D in its ligands (PubMed:1918072). Integrin alpha-V:beta-6 (ITGAV:ITGB6) mediates R-G-D-dependent release of transforming growth factor beta-1 (TGF-beta-1) from regulatory Latency-associated peptide (LAP), thereby playing a key role in TGF-beta-1 activation on the surface of activated regulatory T-cells (Tregs) (Probable). Required during vasculogenesis (By similarity).

Drugs associated with ITGB8

WO2023244547

Patent Mining

Target

ITGB8

Mechanism-

Active Org.

The Regents of the University of California

Originator Org.

The Regents of the University of California

Active Indication

Digestive System Disorders [+8]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2024056668

Patent Mining

Target

ITGB8

Mechanism-

Active Org.

Université Claude Bernard Lyon 1 [+2]

Originator Org.

Centre National de la Recherche Scientifique [+2]

Active Indication

Solid tumor

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

MEDI-8367

Target

ITGB8

Mechanism

ITGB8 inhibitors

Active Org.-

Originator Org.

AstraZeneca PLC

Active Indication-

Inactive Indication

Chronic Kidney Diseases

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with ITGB8

NCT04365218

/ CompletedPhase 1

A Phase I Randomized, Blinded, Placebo-controlled Study to Evaluate the Safety and Pharmacokinetics of MEDI8367 Administered as Single Ascending Doses in Healthy Subjects, and as a Single Dose in Healthy Subjects of Japanese-descent and in Subjects With Chronic Kidney Disease

This Phase I First in Human (FIH) study is being conducted to determine the safety, pharmacokinetics (PK), pharmacodynamics (PD), and immunogenicity profile of MEDI8367 across the dose range.

Start Date22 Jul 2020

Sponsor / Collaborator

AstraZeneca PLC

[+1]

100 Clinical Results associated with ITGB8

100 Translational Medicine associated with ITGB8

0 Patents (Medical) associated with ITGB8

209

Literatures (Medical) associated with ITGB8

01 Jan 2025·Advanced Science

Integrin β8 Facilitates Macrophage Infiltration and Polarization by Regulating CCL5 to Promote LUAD Progression

Article

Author: Zhao, Yanbin ; Song, Lei ; Hou, Zhenxin ; Wu, Yang ; Shao, Yanchi ; Zhang, Yu ; Zhang, Wenwen ; Yang, Chen ; Gao, Yue ; Yu, Xi

AbstractThe tumor microenvironment (TME) influences cancer progression and metastasis. Integrin β8 (ITGβ8), a member of the integrin family, is upregulated in various cancers. In this study, it is determined as a key factor that mediates the interaction between lung adenocarcinoma (LUAD) cells and macrophages. Increased expression levels of ITGβ8 are associated with increased numbers of CD163+ macrophages and poor prognosis in LUAD patients. The overexpression of ITGβ8 in LUAD cells promotes the polarization of THP‐1 macrophages toward the M2 phenotype. In contrast, TCM (conditioned medium from the co‐culture system) from THP‐1 macrophages and ITGβ8‐overexpressing A549 cells promoted the proliferation and invasion of A549 cells. Mechanistically, chemokine (C‐C motif) ligand 5 (CCL5) plays an important role in mediating ITGβ8‐induced macrophage polarization, and the phosphoinositide 3‐kinase (PI3K)/AKT serine/threonine kinase (AKT)/interferon regulatory factor 9 (IRF9) pathway is involved in this process. Moreover, interleukin 8 (IL8) and interleukin 10 (IL10) produced by M2‐like macrophages regulate the expression of ITGβ8 in LUAD cells through the spi‐1 proto‐oncogene (SPI1). This study elucidates the feedback mechanism of ITGβ8 between LUAD cells and macrophages.

31 Dec 2024·Journal of Nutritional Science and Vitaminology

Fructo-Oligosaccharides Enhance the Expression of Genes Related to Focal Adhesion- and Inflammation-Pathways in Small Intestinal Absorptive Caco-2 Cells

Article

Author: ISHIYAMA, Shiori ; HARASAWA, Aya ; MOCHIZUKI, Kazuki

Recently, we demonstrated, using mRNA microarray analysis, that fructo-oligosaccharides (FOS), which are indigestible carbohydrates, enhanced the expression of several inflammation-related genes, such as CLEC7A, CCL2, ITGA2, and F3, by ≥4-fold in Caco-2 cells, a model of human intestinal absorptive cells, independently of intestinal bacteria (Harasawa A et al., Nutrition, 112140, 2023). However, whether FOS enhances the expression of genes in other pathways, particularly the non-inflammatory pathways, in Caco-2 cells has not been investigated. Here, we explored the pathways affected by FOS, based on identification of differentially expressed genes with ≥2-fold change (linear-fold change) in expression upon FOS treatment. Caco-2 cells were cultured for 24 h in high glucose-Dulbecco's modified Eagle medium supplemented with 10% fetal calf serum containing FOS. The differentially expressed genes in these cells, identified using mRNA microarray analysis, were categorized using the pathway analysis and subsequently upregulated genes in typical pathways were subjected to protein network analysis. RT-qPCR was performed to validate the expression of selected genes. Treatment with 10% FOS enhanced the expression of a set of genes, such as ITGB8, ITGA6, SPP1, CAV1, LAMA3, ARHGAP5, and LAMC2, in the focal adhesion pathway. In addition, this treatment increased the expression of many genes involved in various inflammatory pathways, such as TNF, ITGA5, ITGB3, PTGS2, FGF2, FLNC, EDNRB, VEGFA, and MMP13. Protein network analysis showed that genes in the focal adhesion and endothelin pathways induced by FOS were closely associated with each other. FOS treatment of human intestinal absorptive-like cells enhances a set of genes in the focal adhesion and inflammation pathways.

01 Dec 2024·Alzheimer's & Dementia

Cross‐Ancestry Meta‐Analysis of APOE‐ε4 Stratified GWAS of Longitudinal Cognitive Decline in Older Adults

Article

Author: Eissman, Jaclyn M. ; Keene, C. Dirk ; Engelman, Corinne D. ; Walters, Skylar ; Kukull, Walter A. ; Contreras, Alex G. ; Resnick, Susan M. ; Mayeux, Richard ; Regelson, Alexandra N. ; Hohman, Timothy J. ; Ferrucci, Luigi ; Crane, Paul K. ; Mukherjee, Shubhabrata ; Cuccaro, Michael L. ; Saykin, Andrew J. ; Dumitrescu, Logan C. ; Gifford, Katherine A. ; Schellenberg, Gerard D. ; Choi, Seo‐Eun ; Barnes, Lisa L. ; Durant, Alaina ; Schneider, Julie A. ; Trittschuh, Emily H. ; Scollard, Phoebe ; Pericak‐Vance, Margaret A ; Jefferson, Angela L. ; Johnson, Sterling C. ; Bilgel, Murat ; Albert, Marilyn S. ; Lee, Michael L. ; Farrer, Lindsay A. ; Kunkle, Brian W. ; Martin, Eden R. ; Thompson, Paul M. ; Naj, Adam C. ; Bennett, David A. ; Kuzma, Amanda B ; Mez, Jesse ; Bush, William S. ; Haines, Jonathan L. ; Wang, Li‐San ; Cruchaga, Carlos ; Archer, Derek B. ; Sperling, Reisa A

AbstractBackgroundThe Apolipoprotein E ε4 (APOE‐ε4) allele is common in the population, but acts as the strongest genetic risk factor for late‐onset Alzheimer’s disease (AD). Despite the strength of the association, there is notable heterogeneity in the population including a strong modifying effect of genetic ancestry, with the APOE‐ε4 allele showing a stronger association among individuals of European ancestry (EUR) compared to individuals of African ancestry (AFR). Given this heterogeneity, we sought to identify genetic modifiers of APOE‐ε4 related to cognitive decline leveraging APOE‐ε4 stratified and interaction genome‐wide association analyses (GWAS).MethodWe leveraged a comprehensive harmonized cognitive dataset from nine well‐characterized aging and AD cohorts, representing African and European ancestries (total of 32,751 individuals, including 10,969 EUR ε4 carriers, 18,385 EUR non‐carriers, 1,495 AFR ε4 carriers, and 1,902 AFR non‐carriers). We then conducted APOE stratified and interaction GWAS and post GWAS analyses on longitudinal composite measures of memory, executive function, and language. To capture longitudinal cognitive trajectories, linear mixed effects models were employed, focusing on the rate of cognitive decline over time. Post GWAS analysis included eQTL analysis, gene‐set/pathway‐set analysis, and an assessment of genetic correlations.ResultWe identified novel loci for baseline executive function performance including two that are specific to APOE‐ε4 carriers (rs28609108 on chromosome 9 and rs2959641 on chromosome 15) and one that is specific to non‐carriers (rs73072750 on chromosome 7). The effect sizes of these three loci remained consistent when subset by ancestry, achieving statistical significance in EUR, and nominal significance in AFR. Post GWAS eQTL analyses implicate the glutamate receptor subunit gene (GRIN3A) among APOE‐ε4 carriers, while the integrin gene (ITGB8). Additionally, both GRIN3A and ITGB8 have been previously implicated in AD/cognition GWAS, underscoring their relevance in the context of APOE‐ε4.ConclusionOur study has shed light on several novel genetic factors that relate to late‐life cognitive performance in an APOE‐specific manner. These findings enrich our understanding of the genetic landscape influencing cognitive decline. Further research is imperative to unravel how these genetic variations affect biological processes and the potential in guiding therapeutic strategies.

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