Rabbit Anti-Human CD107a
- Known as:
- Rabbit Antibody toHuman CD107a
- Catalog number:
- 129-10091
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human CD107a
Related genes to: Rabbit Anti-Human CD107a
- 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: Rabbit Anti-Human CD107a
Related articles to: Rabbit Anti-Human CD107a
- To investigate the effect of circular RNA LAMP1 (circ-LAMP1) on the malignant progression of acute myeloid leukemia (AML) cells by regulating the miR-194-5p/SALL4 axis. - Source: PubMed
DU Yun-LongZhang YanZhang ChanFu De-Long - Although HSP70 and thioredoxin-1 (TRX1) are well known to counteract methamphetamine (METH)-induced neurodegeneration, no evidence on the effects of METH administration concerning the level, localization, and co-expression of HSP70 and/or TRX1 is available. Therefore, in the present study, carried out using methamphetamine-treated PC12 cells, we sought to analyze these effects along with the merging of specific markers for mitochondria, autophagy, lysosomes, and chaperone-mediated autophagy (CMA). : The levels of specific proteins for specific cell compartments were assessed along with their merging. Thus, co-expression of HSP70 and TRX1 with lipidated LC3 (LC3-II), as well as lysosomal markers such as LAMP1 and LAMP2 (a specific marker for CMA), was assessed. Due to severe mitochondrial alterations produced by METH, both MitoTracker green and MitoTracker red were used in these experimental conditions. Light and electron microscopy, including in situ stoichiometry, were used in these experiments. A moderate dose of METH, 100 µM, increases both TRX1 and HSP70; while HSP70 is preferentially co-expressed with the lysosome marker LAMP1, TRX1 is instead co-expressed with the marker LAMP2, which stains for CMA. Both chaperones increase along with cleaved caspase 3 and the autophagosome marker LC3-II. The outcome of the present study applies to METH-induced intoxication and is relevant in the fields of neurodegeneration, acute neuronal injury, and the domain of drug abuse. In fact, suppression of TRX1 enables METH-induced addiction, while overexpression of TRX1 or HSP70 produces the opposite effect. - Source: PubMed
Publication date: 2026/09/21
Ferrucci MichelaLazzeri GloriaGiambelluca Maria ALenzi PaolaBusceti Carla LFornai Francesco - Prolonged exposure to 1,2-dichloroethane (1,2-DCE) can lead to cognitive dysfunction, and neuronal loss is a proven key driver. In mice, 1,2-DCE exposure reduced hippocampal ATP levels, triggering AMPK phosphorylation, mTOR suppression, and ULK1 activation, along with increased Beclin 1 and LC3-II/I levels, collectively indicating enhanced autophagy initiation. Meanwhile, p62 accumulation and decreased LAMP1 and CTSD expression indicated impaired autophagic degradation, accompanied by increased neuronal apoptosis. Consistent with these in vivo findings, PC12 cells, a neuron-like cell line, exhibited mitochondrial dysfunction after exposure to 2-chloroethanol (2-CE, a metabolite of 1,2-DCE in vivo), as evidenced by ATP depletion, mitochondrial membrane potential loss, and elevated ROS production. Furthermore, 2-CE activated the AMPK-mTOR-ULK1 signaling pathway to initiate autophagy, while also disrupting lysosomal structure and function, leading to impaired autophagic flux and enhanced apoptosis. In conclusion, prolonged 1,2-DCE exposure induces mitochondrial dysfunction and ATP depletion, activating AMPK-mTOR-ULK1-mediated autophagy initiation. Meanwhile, concomitant lysosomal damage impairs autophagic degradation, and the combined effect promotes neuronal apoptosis. These findings suggest a potential strategy for preventing and treating 1,2-DCE-induced cognitive impairment. - Source: PubMed
Publication date: 2026/09/09
Luo ZhenlinWang ChenWang ChuntingWang GaoyangCui WantingWang ZijiangZhao Fenghong - Berberine (BBR), a natural isoquinoline alkaloid, has been shown to specifically bind to sirtuin 2 (SIRT2) and exhibit anticancer activity. This study aimed to elucidate the therapeutic mechanisms of BBR in non-small cell lung cancer (NSCLC). - Source: PubMed
Publication date: 2026/09/25
Wu MingliangYang GuobiaoYang JianyeXu Mengmin - is an intracellular pathogen whose cell cycle encompasses attachment, internalization, trafficking, replication, and egress from host cells. Although the intracellular life of has been extensively studied, the mechanisms underlying its exit from host cells remain unclear. In this work, we expand the knowledge of this intracellular step by observing a significant increase in the formation of -containing vacuoles with autophagic features (aBCVs) and abundant extracellular clusters (BECs) after 72 h of infection. Membrane extensions protruding through actin polymerization were evident in cells at later stages of infection. Purified aBCVs and BECs were similar in size and predominantly acidic. These vacuoles exhibited a compact arrangement of well-ordered bacteria, comprising a heterogeneous population of dead and live bacteria and host components, including LAMP-1 and actin filaments. A proportion of BECs were enclosed within an impermeable host membrane, while others were not. The actin cytoskeleton was implicated in the protrusion of BECs, since modulation of Rho GTPases affected intracellular aBCV formation and the egress of BECs. BECs protruding from cells invaded uninfected cells, initiating a new cycle of infection. The topological structure and function of BECs underscore their significance in the life cycle as vehicles for bacterial dissemination to host cells and organs.IMPORTANCE is an intracellular pathogen that traffics to the endoplasmic reticulum, where it replicates. However, the mechanisms by which exits host cells and infects new ones remain poorly understood. Our findings reveal that protruding acidic autophagic-like vesicles containing compact, well-organized clusters are shed from cells via the GTPase-dependent recruitment of actin filaments. Through this process, the vesicles are impermeable to antibodies and other substances, like antibiotics, and are highly infectious to neighboring cells. This mechanism enhances the understanding of the well-known stealth strategy to evade the immune system and establish harmful, long-lasting infections. - Source: PubMed
Publication date: 2026/09/24
Campos-Godínez José FabioHernández-Saborío AlejandroVargas-Moya TiffanyGómez-Vargas ValeriaEspinoza-Villagra DavidSandoval IgnacioRojas-Salas María PaulaLópez-Hernández MelanyVega-Arce RodrigoPereira-Reyes ReynaldoPrado MonicaChacón-Díaz CarlosMoreno EdgardoChaves-Olarte EstebanAltamirano-Silva Pamela