Ask about this productRelated genes to: LASP1 Blocking Peptide
- Gene:
- LASP1 NIH gene
- Name:
- LIM and SH3 protein 1
- Previous symbol:
- -
- Synonyms:
- MLN50, Lasp-1
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-22
- Date modifiied:
- 2016-10-05
Related products to: LASP1 Blocking Peptide
Related articles to: LASP1 Blocking Peptide
- Human-virus protein-protein interactions (PPIs) govern critical steps in viral entry, replication, and immune modulation. Despite their importance, the physicochemical determinants underlying human-virus interface recognition remain incompletely understood. A detailed characterization of these determinants is essential for uncovering viral hijacking mechanisms and enabling therapeutic targeting. To address this, we developed a sequence-based deep learning framework, HVIface, for residue-level prediction of human-virus PPI interfaces. - Source: PubMed
Publication date: 2026/05/08
Gupta Krishna KantVijayvargiya MontyPaul GeethaPhilip Ninan SajeethChauhan Radha - LIM and SH3 protein 1 (LASP1) plays a crucial role in tumorigenesis and metastasis, but its function in bladder cancer remains unclear. Here, we found that LASP1 was markedly upregulated in bladder cancer tissues and correlated with poor prognosis. Co-immunoprecipitation and mass spectrometry identified MYH9 as a direct LASP1-binding partner, with the interaction mediated by the SH3 domain of LASP1 and the M2 domain of MYH9. Functional assays revealed that LASP1 maintained mitochondrial morphology and function by regulating MYH9, thereby preventing mitochondrial damage-induced apoptosis and promoting cell proliferation and migration. In vitro and in vivo experiments consistently demonstrated that the LASP1-MYH9 axis enhances bladder cancer growth and metastasis. Overall, our findings reveal that LASP1 facilitates bladder cancer progression by interacting with MYH9 to inhibit mitochondria-mediated apoptosis, and provide a rationale for further exploring the LASP1-MYH9 axis in bladder cancer therapy. - Source: PubMed
Publication date: 2026/05/09
Wang KeHu ZeweiZhu YihaoPiao ChiyuanShi YuchenJing HongweiLi LinLiu Tao - Non-small cell lung cancer (NSCLC) is a major cause of cancer-related mortality globally, linked to an immunosuppressive microenvironment. Circular RNA circSPARC is crucial in cancer, but its function in NSCLC remains unclear. 66 NSCLC tissue samples and 4 cell lines were analyzed for circSPARC and PD-L1 expression via qRT-PCR. A549 and H1299 cells were transfected with shRNA targeting circSPARC. THP-1 cells were differentiated into macrophages with phorbol 12-myristate-13-acetate (PMA). A549 and H1299 cells were co-cultured separately with CD8T cells. Cell viability, invasion, expression of M2 macrophage markers (CD206, CD163), immune checkpoint (PD-L1), cytokines (IL-10, TGF-β, IFN-γ, TNF-α), and the proportion of CD8 TNF-α T cells were analyzed by CCK-8 assay, Transwell, Western blot, ELISA, and flow cytometry. Dual-luciferase reporter and RNA pull-down assays were employed to confirm interactions between circSPARC, miR-199a-5p, and LASP1. Rescue experiments involved inhibiting miR-199a-5p or by overexpressing/silencing LASP1. Finally, the role of circSPARC was investigated in vivo using a subcutaneous tumor model. CircSPARC was highly expressed in NSCLC tissues and cells. circSPARC knockdown inhibited NSCLC cell viability, invasion, and reduced CD206 and CD163 expressions. Moreover, circSPARC knockdown reduced the excretion of immunosuppressive cytokines (IL-10 and TGF-β) as well as PD-L1 expression but promoting release of effector cytokines (IFN-γ and TNF-α) and increasing the proportion of CD8 TNF-α T cells. Mechanistically, circSPARC sponged miR-199a-5p to upregulate LASP1. These findings were validated in a mouse xenograft model. The circSPARC/miR-199a-5p/LASP1 axis mediated the immunosuppressive microenvironment of NSCLC, highlighting circSPARC as a potential therapeutic target. - Source: PubMed
Publication date: 2026/03/18
Zhang ChengshengLuo JingruZhuang XiaohongQin QiXu JunnvLin ShuTang Wenjun - Diabetic kidney disease (DKD), a prevalent complication of diabetes, is the leading cause of chronic kidney disease globally. The current standard of care cannot halt disease progression and thus new therapeutic targets are needed. We previously showed that the metalloprotease ADAM17 mediates the profibrotic response to high glucose in kidney mesangial cells. Its upregulation in high glucose conditions augments its profibrotic effects. Here we investigate regulation of the Adam17 promoter region -2304/-1567, previously shown to be glucose responsive, for which regulatory factors have not yet been identified. - Source: PubMed
Publication date: 2026/02/06
Trink JackieGao BoLi RenzhongPatel Jaina HBajwa UroojZernecke AlmaButt ElkeKrepinsky Joan C - Acute lung injury (ALI)/Acute Respiratory Distress Syndrome (ARDS) is a life-threatening condition marked by severe inflammatory responses and disruption of the alveolar-capillary barrier, leading to high mortality rates and lack of effective treatments. Recent research has underscored the crucial role of programmed cell death pathways-pyroptosis, apoptosis, and necroptosis-in exacerbating inflammation and barrier dysfunction in ALI/ARDS. However, effective therapeutic agents targeting this process remain scarce. In this study, we reveal that PANoptosis, which integrates these cell death pathways through the PANoptosome complex, plays a central role in the pathogenesis and progression of ALI/ARDS. The levels of PANoptosis-related molecules were significantly elevated in both the ALI mice and the clinical ARDS patient samples, highlighting it as a novel therapeutic target. Building on this insight, we developed a multifunctional nanomedicine, TPNs/Sal B, which integrates tea polyphenol-based nanoparticles (TPNs), a bioactive nanomaterial with anti-pyroptotic and anti-necroptotic properties, with salvianolic acid B (Sal B), known for its anti-apoptotic effects. Our results demonstrate that the nanomedcine TPNs/Sal B effectively inhibit PANoptosis, thereby attenuating lung tissue pathological damage, reducing inflammation, and improving lung epithelial barrier function in ALI models. Moreover, we identified LIM and SH3 protein 1 (LASP1) which may play an critical role in modulating alveolar epithelial barrier function during ALI/ARDS progression, and treatment with TPNs/Sal B effectively restored LASP1 levels. Our findings underscore the therapeutic potential of TPNs/Sal B as a targeted treatment for ALI/ARDS, offering a promising strategy for modulating PANoptosis and preserving lung function. - Source: PubMed
Publication date: 2025/12/26
Cui YanhuiWang XueqinLu CaiyangRan LilingGuo ZiruiYao JiayuYu TianLiu XuanxiLi FangLi ChangqiMeng YingcaiZhou Wenhu