Ask about this productRelated genes to: Gja4 Blocking Peptide
- Gene:
- GJA4 NIH gene
- Name:
- gap junction protein alpha 4
- Previous symbol:
- -
- Synonyms:
- CX37
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-11
- Date modifiied:
- 2016-10-05
Related products to: Gja4 Blocking Peptide
Related articles to: Gja4 Blocking Peptide
- Although follicular development and oocyte competence depend on insulin-like growth factor-1 (IGF-1), its optimal dose and molecular mechanisms during goat maturation (IVM) remain unclear. - Source: PubMed
Publication date: 2026/05/29
Widjiati WidjiatiLuqman Epy MuhammadDarsini NinikAulanni'am Aulanni'amHendrawan Viski FitriKurniawati Devia YoanitaJaafar Wan Nor Fitri Bin Wan - We examined gene expression profiles in abdominal aortic aneurysm (AAA) lesions . normal aortas by cDNA microarray and real-time quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR). - Source: PubMed
Lu SongLi Li PingWhite John VZhang XiaoyingNwaneshiudu IfeyinwaNwaneshiudu AdaobiNtaoula NectariaGaughan JohnMonos Dimitri SLin Wan-LuSolomides Charalambos COleszak Emilia LPlatsoucas Chris D - Colorectal cancer (CRC) shows strong heterogeneity in tumor microenvironment (TME) dynamics, but the mechanisms that shape epithelial-stromal crosstalk are still unclear. Here we focus on A-kinase anchor protein 12 (AKAP12) and Leiomodin 1 (LMOD1) and test a compartment-dependent model in which this program aligns with tight-junction features in epithelium but with a fibrotic, immune-suppressive program in stroma. Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) were employed to profile gene expression patterns in CRC tissues. Immunohistochemistry (IHC) and multiplex immunofluorescence (mIF) validated protein expression and localization. Cell-cell communication analysis and trajectory inference were used to dissect spatial interaction networks. Functional experiments were employed to validate the role of the AKAP12-LMOD1 axis in CAFs in regulating ECM remodeling and antitumor immunity. AKAP12-LMOD1 exhibited a compartment-dependent pattern in CRC. In ACTA2⁻ epithelial regions, the epithelial AKAP12-LMOD1 signal was lower in tumors than in matched normal epithelium and showed a positive association with the tight-junction marker CLDN1. In ACTA2⁺ stromal regions, AKAP12-LMOD1 was enriched, positively associated with the gap-junction marker GJA4, and higher in tumor stroma than matched normal stroma. In a CAF-macrophage non-contact co-culture model, AKAP12 overexpression supported CAF activation and collagen deposition, and shifted macrophages toward an M2-like phenotype; LMOD1 knockdown or SB-431542 partially reversed these effects. Stromal AKAP12-LMOD1-enriched regions also aligned with fibrosis- and M2-related features, and these stromal patterns were prominent in mucinous carcinoma. This study defines AKAP12-LMOD1 as a compartment-dependent stromal program in CRC that links ACTA2⁺ stroma to gap-junction features, fibrosis, and M2-like macrophage polarization, while showing a distinct epithelial association with tight-junction features. These findings support a stroma-centered working model for AKAP12-LMOD1 in CRC microenvironmental heterogeneity and suggest that stromal modulation of this program, together with targeting fibrosis and M2-like immune features, may be explored as hypothesis-level, subtype-oriented therapeutic directions in stroma-rich CRC. - Source: PubMed
Publication date: 2026/04/20
Ye Qian-WenLiu Yuan-JieXu GuoChen Yu-GenLi Jie-Pin - Breast cancer-related lymphedema (BCRL) remains a major chronic complication following axillary lymph node dissection (ALND), particularly in regions where locally advanced breast cancer is prevalent. While several clinical factors have been identified, the role of genetic predisposition in BCRL development remains underexplored. This study aimed to identify genetic and clinical factors associated with the development of BCRL, focusing on the Gap Junction Protein Alpha-4 (GJA4) rs705193 mutation as a potential biomarker. - Source: PubMed
Publication date: 2026/02/17
Putri Rizky IfandrianiSutandyo NoorwatiSiregar Nurjati ChairaniWanandi Septelia InawatiHarimurti KuntjoroHernowo Bethy SBrahma BayuPerdana Adhitya BayuWidiasti InnasSari Erin KurniaPanigoro Sonar Soni - We investigated whether basement membrane (BM) laminins influence regional differences in the vasculature by performing single-cell RNA sequencing on cerebral blood vessels from mice lacking the major vascular laminins in endothelial and smooth muscle BMs, laminin α4 ( ) and laminin α5 (), and wild-type littermates. Our dataset expands existing cerebral vascular transcriptomic profiles and reveals that endothelial cells exhibit increased arterial marker expression and reduced postcapillary venule identity. In vitro and in vivo studies indicated that compensatory upregulation of laminin α5 in vessels enhances expression of junctional proteins (, ) and promotes vessel contractility via increased expression of contractile molecules in mural cells. Additionally, loss of upregulated expression of large artery markers (, , ) and resulted in elevated autotaxin () levels, a key enzyme in lysophosphatidic acid production implicated in stroke. Accordingly, mice exhibited worsened stroke outcomes, driven not by immune infiltration or junctional defects, but by increased vascular permeability likely mediated by autotaxin and/or activation of resident myeloid cells. Our data suggest that laminin α4/α5 ratios in vascular BMs affect functional zonation between arterioles, capillaries and postcapillary venules by modulating metabolic pathways in endothelial and mural cells, and indirectly influencing resident myeloid cells. - Source: PubMed
Publication date: 2026/02/16
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