Ask about this productRelated genes to: CD107a antibody
- Gene:
- LAMP1 NIH gene
- Name:
- lysosomal associated membrane protein 1
- Previous symbol:
- -
- Synonyms:
- CD107a
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-15
- Date modifiied:
- 2016-01-14
Related products to: CD107a antibody
Related articles to: CD107a antibody
- Toxin A and B from Clostridioides difficile are the main pathogenicity factors for clinical symptoms of C. difficile infections. Receptor-mediated endocytosis and endosomal escape are required for targeting substrate proteins of the Rho-GTPase family. We previously reported that Toxin B (TcdB) affects endo-lysosomal transport and autophagic flux of target cells. These effects are independent from pathogenic Rho inhibition. Here, we aimed at further characterization of this event by immunofluorescent characterization of the vesicular structures that are affected. We found large aggregates of damaged endolysosomal structures positive for EEA1, LAMP1, CHMP4B and TcdB, as well as an increase in perinuclear concentration of non-mature autophagosomes (amphisomes) positive for SQSTM, Rab7, and LC3B. We investigated whether Rab7, a regulator of late endosome transport, is causative for decreased lysosome function. Although TcdB induced an increase in active Rab7, as tested by an RILP pull-down assay, inhibition of Rab7 did not prevent TcdB-induced decrease in cathepsin D as a surrogate for lysosome dysfunction. It also indicates that the observed increase in Rab7 positive amphisomes is secondary to lysosomal dysfunction. By applying an autoproteolytic deficient mutant of TcdB we proved that the release of the glucosyltransferase domain is mandatory for triggering all of these effects. This suggests that after membrane perforation the toxin remnants leave an open leak in endolysosomes affecting ion homeostasis. Investigation of all large clostridial glucosyltransferases and other toxins revealed lysosomal dysfunction as a general effect of many but not of all toxins that integrate into the endosome membrane. - Source: PubMed
Publication date: 2026/04/15
Langejürgen AnnaSchmidt GudulaUnsöld LeonTatge HelmaOyson EthelGerhard Ralf - Niemann-Pick type C disease (NPCD) is a rare and fatal lysosomal storage disorder. There are limited therapies for NPCD, although multiple small-molecule compounds have shown therapeutic potential for NPCD. Curcumin (CUR), a polyphenolic compound enriched in turmeric, has cholesterol-lowering effects via regulating intestinal cholesterol absorption and liver cholesterol synthesis. CUR normalises sphingolipid trafficking and stimulates exosome/microvesicle release, increases cytosolic Ca levels, and enhances lysosomal activation via mTOR suppression and TFEB activation. How CUR specifically targets lysosomal cholesterol has not been fully clarified. - Source: PubMed
Publication date: 2026/04/26
Chen HongyuZhao MengliLuo YuChu XiaoheLi Dan - This study investigated the molecular mechanism by which FAM134B regulates endoplasmic reticulum stress (ERS) and autophagy to promote thyroid carcinoma (THCA) development. FAM134B expression in clinical THCA samples was examined. FAM134B expression was knocked down in TPC-1 cells, while FAM134B was overexpressed in KTC-1 cells. Cell proliferation and apoptosis were determined. Cleaved caspase-3 (C-Casp-3), caspase-12, and unfolded protein response markers were detected. LC3B fluorescence expression and Calnexin-LAMP1 co-localization were assessed. FAM134B was highly expressed in THCA, and its overexpression was significantly associated with higher T staging. Knocking down FAM134B reduced THCA cell proliferation and encouraged apoptosis, while its overexpression resulted in contrary effects. FAM134B knockdown activated ERS (upregulating p-PERK/PERK, p-IRE1α/IRE1α, and CHOP) and enhanced autophagy (increasing LC3-II/I expression levels, decreasing p62 expression levels, and enhancing Calnexin-LAMP1 colocalization). Inhibition of ERS partially reversed the suppression of malignant biological behavior in THCA cells caused by FAM134B knockdown. FAM134B acts as an oncogene in THCA. Silencing FAM134B inhibits THCA cell proliferation and promotes apoptosis by inducing ERS and autophagy. - Source: PubMed
Publication date: 2026/04/14
Cheng TingtingShu JiaoZhou ChengLi LiXiang Quan - While the uptake of cargos via endocytosis and the subsequent trafficking through the cell is crucial for normal cellular function and tightly regulated, the study of this bears challenges. Most studies of Rab GTPases, the primary coordinators of endocytic progression, rely on ectopic expression of fluorescently tagged proteins via transient transfection. Previous studies already showed that the design of the fluorescent tag as well as the unpredictable nature of transient transfection can cause problems. Even though the pitfalls of overexpression have been reported for several research fields, the consequences of overexpression on endocytic trafficking are under-reported. To highlight the importance of working with endogenous levels of proteins to draw conclusions about endosome colocalization and identity, we present an example where the colocalization of two endosomal regulators/markers, Rab11 and LAMP1, varied drastically when these proteins were analyzed at their endogenous levels or following ectopic expression. When both proteins were ectopically expressed, up to 90% colocalization was observed. However, when analyzed at the endogenous level no colocalization was detectable. This study shows how important vesicular trafficking perturbation can occur following ectopic expression of endosomal proteins. - Source: PubMed
Publication date: 2026/04/22
Hornfeck SarahTrofimenko EvgeniyaWidmann Christian - Schizophrenia (SZ) is characterized by immune dysregulation and decreased autophagy. However, the mechanistic interplay between these two processes remains unclear. This study aimed to explore the relationship between autophagy and inflammation in SZ patients and a maternal immune activation (MIA)-induced SZ mouse model. Autophagic activity and inflammatory markers were assessed in peripheral blood mononuclear cells (PBMCs) from SZ patients and healthy controls using flowcytometry, Western blotting, and qPCR. Cytokine modulation experiments were conducted in vitro to determine causal relationships. Behavioral, molecular, and neurochemical analyses were performed in MIA-induced SZ-like mice, with or without mTOR inhibitor rapamycin treatment, to assess the role of mTOR-regulated autophagy in vivo. SZ patients exhibited reduced autophagic-lysosome function in PBMCs, evidenced by decreased monodansylcadaverine-positive cells, Beclin-1, LC3B/LC3A, LAMP1, and cathepsin D, alongside increased p62 levels, accompanied by hyperactivation of the PI3K/AKT/mTOR pathway and ULK1 inhibition. These changes were associated with elevated inflammatory markers, including IL-1β, IL-6, IFN-γ, and NLRP3 inflammasome components (NLRP3, ASC, caspase-1). Pharmacological inhibition of autophagy further amplified inflammatory gene expression in vitro, while IL-10 treatment restored LC3B expression, which suppressed by IL-1β/IL-6. MIA mice showed SZ-like behaviors, reduced hippocampal Beclin-1, glial polarization imbalance, cortical neuroinflammation, and monoaminergic disruptions. Rapamycin-induced mTOR inhibition restored autophagy and reversed these abnormalities. Our findings demonstrated that hyperactivation of mTOR suppressed autophagy, leading to sustained elevation of pro-inflammatory cytokines in SZ. Inhibition of mTOR restored autophagic activity, thereby reducing neuroinflammation and glial pro-inflammatory activation, suggesting autophagy as a promising therapeutic target for SZ. - Source: PubMed
Publication date: 2026/04/20
Yan LingWang XiaonaZhang YongpingYan HaifengLin ZhixiongZhang LiqiangZhang CaiSong Cai