Ask about this productRelated genes to: LAMA4 antibody
- Gene:
- LAMA4 NIH gene
- Name:
- laminin subunit alpha 4
- Previous symbol:
- -
- Synonyms:
- LAMA3
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-26
- Date modifiied:
- 2019-04-23
Related products to: LAMA4 antibody
Related articles to: LAMA4 antibody
- Periodontitis-induced inflammatory microenvironment compromises the function of periodontal ligament stem cells (PDLSCs) and significantly impedes the regeneration of periodontal tissues. Meanwhile, the clinical application of extracellular vesicles (EVs) is constrained by their low yield and high production costs. For the first time, this study systematically compares the functional differences between intracellular vesicles (IVs) and EVs derived from human PDLSCs (hPDLSCs) in promoting bone regeneration under inflammatory conditions, while also elucidating their underlying molecular mechanisms. IVs were produced with 6.9-fold higher efficiency and exhibited superior cellular uptake compared to EVs. In vitro, under lipopolysaccharide (LPS)-induced inflammatory environment, IVs outperformed EVs in enhancing the hPDLSCs proliferation, suppressing the secretion of pro-inflammatory cytokines (IL-6 and TNF-α) and upregulating osteogenic markers through Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) activation, thereby promoting calcium nodule formation. Proteomic and functional analyses identified laminin subunit alpha 4 (LAMA4) as a key effector enriched in IVs, which is essential for activating YAP/TAZ signalling and osteogenesis. Correspondingly, in vivo, IVs-loaded gel effectively promoted bone regeneration in rat periodontal bone defects without organ toxicity. This study establishes IVs as a superior, high-yield cell-free therapeutic and delineates an LAMA4-dependent mechanism via YAP/TAZ activation for inflammatory bone regeneration. - Source: PubMed
Liu HaotianWu YuWang QunyiZhang TingTong XinYan FuhuaZhang Qian - Energy balance (EB) can be an important health indicator in dairy cows, as a severe or prolonged period of negative energy balance is a key risk factor for metabolic disorders, impaired immune function, and reduced fertility. Understanding the biological mechanisms of energy balance is fundamental to developing strategies that improve energy intake, mitigate negative energy balance, and enhance the management of metabolic challenges in dairy cows. This study employed whole blood transcriptomic as a scalable approach to unravel the molecular networks governing EB in early-lactation Holstein cows. Whole blood RNA-Seq analysis during early lactation (24-32 d post calving) identified 26 differentially expressed genes associated with EB. These genes were found to be engaged in pathways critical to metabolic adaptation, including PPAR signaling (PRDM16), extracellular matrix organization (COL18A1, EMID1), and cell fate commitment (SOX13, WNT5A). Weighted gene co-expression network analysis identified a key module (87 genes) strongly correlated with EB. Protein-protein interaction networks further connected DBN1 to cytoskeletal signaling (L1CAM, AMPH) and COL18A1 to WNT-integrin signaling (LAMA4, PTK2), suggesting novel mechanisms for systemic stress adaptation. These findings advance the understanding of EB as a polygenic trait characterized by multi-tissue interactions and proposes actionable markers that can be applied to dairy cow management as targets for genetic selection to improve metabolic resilience. Future work will seek to validate these findings using tissue-specific analyses, and functional assays to elucidate mechanistic roles of prioritized genes. - Source: PubMed
Publication date: 2026/03/16
Jiang WentaoKaitholil Steffimol Rose ChackoRazban VahidFerris ConradMooney Mark HShirali Masoud - Molecular characterization of balanced complex chromosomal rearrangements (CCR) aids in understanding the pathophysiological mechanism and corresponding genotype-phenotype correlations. The present case describes a male child with intellectual disability, developmental delay, and dysmorphism. A thorough and sequential genetic evaluation using karyotyping, fluorescence in situ hybridization (FISH), chromosomal microarray (CMA), and long read sequencing (LRS) identified a genomically balanced CCR. The CCR involved eight chromosomes, the largest to be documented till date for chromoanagenesis and being balanced despite the high level of complex chromosomal involvement. Translocations accounted for the majority of the rearrangements along with an insertion, inversion, and a small deletion likely driven by chromoplexy. Although the CCR was genomically balanced, it may still result in functionally significant genomic consequences including gene disruptions, gene fusions, and position effects. Long read whole genome sequencing using PacBio was used for breakpoint characterization that revealed three protein-coding genes to be disrupted, namely, NLGN4X, LAMA4, and ALG6. Of these, a candidate association was observed for the NLGN4X gene with the intellectual disability phenotype reported in the proband, which is likely due to disruption of transcription and nonsense mediated decay. We show combinatorial application of advanced genomic technologies with orthogonal cytogenetic techniques in delineating balanced CCRs and understanding the biological and potential clinical implications of balanced yet functionally disruptive CCRs. - Source: PubMed
Publication date: 2026/02/27
Sheth FrennyShah JhanviMuranjan MamtaLiehr ThomasPadutsch NiklasMane SrikantNg Sok Meng EvelynLi PeiningDesai ManishaKansara HenySheth Jayesh JSheth Harsh - 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
Deshpande TusharKapupara KishanHannocks Melanie-JaneHuppert JulaSamawar Sai-KiranThulichery Devika RagBudny SigmundGhavampour SharangSong JianMeng LingzhangAdams Ralf HJeong Hyun-WooWachsmuth LydiaFaber CorneliusSoltwisch JensHallmann RupertSorokin Lydia - The aggressive metastatic propensity of advanced clear cell renal cell carcinoma (ccRCC) originates from intratumoral heterogeneity. Through integrated single-cell and spatial multi-omics profiling, we identified a FOXC2 tumor subpopulation endowed with vasculogenic mimicry capability as pivotal effector cells driving metastasis. Mechanistically, the transcription factor FOXC2 binds the promoter region of LAMA4 to activate its expression, initiating metastatic cascades via vasculogenic mimicry remodeling. In orthotopic lung metastasis models, FOXC2 tumor cells leveraged LAMA4 to reshape the pulmonary metastatic niche, thereby reinforcing distant metastatic dissemination. Tumor-secreted LAMA4 engaged macrophage surface receptor ITGA6 to trigger GATA3 activation and reprogram macrophages toward a pro-metastatic and immunosuppressive phenotype. Disruption of LAMA4-ITGA6 binding substantially attenuated FOXC2-LAMA4-mediated metastatic burden. These results reveal a novel mechanism by which FOXC2 tumor cells promote metastasis in advanced ccRCC and further establish the therapeutic potential of targeting FOXC2-LAMA4 in blocking the metastatic cascade of ccRCC. - Source: PubMed
Publication date: 2026/01/29
Yao JiaxiXu TongWang ChengyuanWang ChenyuanXie JunfengZheng RuiWang KeJiang XingzuoHu ZeweiJing HongweiLi LinLiu Tao