| 2016 |
In zebrafish, Itga8 (expressed in facial mesenchyme) and Fras1 (expressed in epithelia) function together in epithelial-mesenchymal interactions during pharyngeal pouch morphogenesis; itga8 mutants display defective outpocketing of the first pharyngeal pouch and skeletal defects phenotypically similar to fras1 mutants, consistent with both proteins acting within the same Fraser protein complex. |
Forward mutagenesis screen, CRISPR allele generation, double-mutant analysis, in situ hybridization for expression domains, phenotypic comparison |
Developmental biology |
High |
27265864
|
| 2016 |
In the unilateral ureteral obstruction model, Itga8 deficiency leads to increased phospho-SMAD2/3-positive cells and more α-smooth muscle actin-positive fibroblasts in the tubulointerstitium, as well as enhanced macrophage and T-cell infiltration, indicating that Itga8 attenuates renal interstitial fibrosis by suppressing TGF-β/SMAD signaling and fibroblast activation rather than by regulating cell turnover or apoptosis. |
Knockout mouse model (Itga8-/-) with UUO, immunohistochemistry for phospho-SMAD2/3, α-SMA, macrophage and T-cell markers; proliferation and apoptosis assays |
PloS one |
Medium |
26938996
|
| 2022 |
Itga8-CreER knock-in mice drive tamoxifen-dependent recombination preferentially in vascular smooth muscle cells (but not visceral SMCs), and Srf knockout using this driver causes vascular contractile incompetence and failure to mount angiotensin II-induced blood pressure elevation, placing Itga8 expression in vascular SMCs upstream of SRF-dependent contractile gene regulation. |
Knock-in Cre mouse generation, tamoxifen induction, comparison with Myh11-CreER, conditional Srf knockout, blood pressure measurement, contractility assays |
Nature cardiovascular research |
High |
36424917
|
| 2023 |
Using the Itga8-CreER model to delete YAP and TAZ in smooth muscle cells, YAP/TAZ were found to regulate myocardin (Myocd) expression and SRF levels in bladder detrusor, which in turn drives contractile gene expression, smooth muscle-specific splicing, and bladder contractility; loss of YAP/TAZ reduced cholinergic receptor expression and impaired carbachol- and myosin phosphatase inhibitor-induced contraction. |
Itga8-CreER-mediated conditional deletion of YAP/TAZ in adult mice, RT-qPCR, Western blot, gel contraction assay, constitutively active YAP overexpression in HEK293 cells |
American journal of physiology. Cell physiology |
High |
37927241
|
| 2025 |
In neurogenic bladder fibrosis, Itga8+ fibroblasts coordinate cytoskeletal remodeling via the FAK/RhoA/ROCK signaling axis; Trem2+ macrophage-secreted Fn1 engages Itga8 on fibroblasts to activate them, and conditional deletion (Col1a2-CreERT; Itga8fl/fl) or local Itga8 knockdown attenuates collagen deposition and restores voiding efficiency. |
Single-cell RNA sequencing, conditional knockout (Col1a2-CreERT; Itga8fl/fl), AAV-mediated knockdown in vivo, macrophage depletion experiments, pathway analysis |
Advanced science |
High |
41355531
|
| 2025 |
In hepatic stellate cells (HSCs), ITGA8 expression is upregulated during liver fibrosis and promotes ECM accumulation; AAV2/6-mediated silencing of Itga8 in HSCs reduces fibrosis markers (α-SMA, collagen I), decreases inflammatory cytokines, and suppresses COL11A1 expression as identified by proteomics, implicating ITGA8 in ECM cross-linking via COL11A1 regulation and reducing HSC-mediated collagen contraction. |
CCl4 mouse fibrosis model, AAV2/6-shItga8 selective silencing, in vitro ITGA8 knockdown with proteomic analysis, Sirius Red staining, collagen contraction assay |
Biochemical and biophysical research communications |
Medium |
40056500
|
| 2025 |
ITGA8 sensitizes lung adenocarcinoma cells to EGFR-TKIs (abivertinib) by attenuating the downstream FAK/SRC/AKT/MAPK signaling pathway; ITGA8 knockdown enhanced proliferation, migration, and invasion of H1975 cells and increased tumor growth in xenografts, while overexpression in resistant cells (H1975/ABIR) reduced malignant phenotypes and enhanced drug sensitivity. |
Genome-wide CRISPR-Cas9 screen, ITGA8 knockdown and overexpression, western blot for FAK/SRC/AKT/MAPK pathway, H1975 xenograft mouse model |
Acta pharmacologica Sinica |
Medium |
39809840
|
| 2026 |
ITGA8 overexpression in lung adenocarcinoma suppresses aerobic glycolysis (reducing ECAR, glucose uptake, lactate production) by activating the AMPK signaling pathway and inhibiting the mTOR/S6K/4EBP1 axis; AMPK inhibition reversed ITGA8-mediated glycolysis suppression and restoration of malignant phenotypes, establishing ITGA8 as a metabolic gatekeeper. |
ITGA8 overexpression in LUAD cells, Seahorse metabolic assays (ECAR), glucose/lactate measurements, AMPK inhibitor rescue experiments, in vivo xenograft models, western blot for mTOR/S6K/4EBP1 |
Scientific reports |
Medium |
41731056
|
| 2021 |
ITGA8-positive cells isolated from human trabecular meshwork display properties of Schlemm's canal (SC) endothelial cells: enhanced expression of SC biomarkers, reduced dexamethasone-inducible myocilin secretion, and stronger endothelin 1-induced contractility compared to ITGA8-negative cells, indicating ITGA8 marks a functionally distinct SC-like population involved in aqueous humor outflow resistance. |
Fluorescence in situ hybridization, immunofluorescence, magnetic bead-based cell sorting, flow cytometry, RT-PCR, Western blot, gel contraction assay |
Life sciences |
Medium |
33961857
|
| 2025 |
RAGE regulates cell adhesion through upregulation of ITGA8; the intracellular (cytoplasmic) domain of RAGE is required for modulating cell spreading and for ITGA8 regulation, indicating a signaling link from RAGE's cytoplasmic domain to ITGA8-mediated adhesion to extracellular matrix proteins. |
RAGE domain deletion constructs, cell adhesion assays, cell spreading assays, protein expression analysis |
Cells |
Low |
41294858
|
| 2020 |
In ER-positive breast cancer cells, ITGA8 is silenced by promoter hypermethylation; treatment with 5-aza-2'-deoxycytidine restores ITGA8 protein expression, but this restoration is abolished by 17-beta-estradiol (ERα agonist), indicating that ERα-dependent signaling promotes ITGA8 methylation and silencing in ER-positive breast cancer. |
Methylation-specific PCR, Western blot, 5-aza-dC demethylation treatment, 17-beta-estradiol treatment, clinical tissue methylation analysis |
Annals of translational medicine |
Medium |
32953793
|
| 2024 |
In ovarian cancer, M2 macrophage-derived exosomes deliver circTMCO3, which acts as a competing endogenous RNA for miR-515-5p, thereby reducing miR-515-5p abundance and upregulating ITGA8; miR-515-5p directly downregulates ITGA8, and ITGA8 overexpression reverses the reduced oncogenic activity caused by circTMCO3 silencing, placing ITGA8 downstream of the circTMCO3/miR-515-5p axis in promoting ovarian cancer malignancy. |
Exosome isolation, circRNA knockdown, miRNA mimic/inhibitor experiments, luciferase reporter assay (implied by competing endogenous RNA mechanism), in vivo nude mouse xenograft |
Communications biology |
Low |
38755265
|