mLST8 (L17) Antigen Human Immunized Animal Rabbit poly IgG, serum Antigen peptide
- Known as:
- mLST8 (L17) Antigen Human Immunized Animal Rabbit poly Immunoglobulin G, blood serum Antigen short protein sequence
- Catalog number:
- 28013
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Demeditec
- Gene target:
- mLST8 (L17) Antigen Human Immunized Animal Rabbit poly IgG serum peptide
Related genes to: mLST8 (L17) Antigen Human Immunized Animal Rabbit poly IgG, serum Antigen peptide
- Gene:
- ARL17A NIH gene
- Name:
- ADP ribosylation factor like GTPase 17A
- Previous symbol:
- ARF1P2, ARL17P1
- Synonyms:
- -
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-07
- Date modifiied:
- 2017-07-14
- Gene:
- ARL17B NIH gene
- Name:
- ADP ribosylation factor like GTPase 17B
- Previous symbol:
- ARL17
- Synonyms:
- -
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2007-03-19
- Date modifiied:
- 2015-11-19
- Gene:
- FAM215B NIH gene
- Name:
- family with sequence similarity 215 member B
- Previous symbol:
- -
- Synonyms:
- ARL17A-IT1
- Chromosome:
- 17q21.31
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2011-12-08
- Date modifiied:
- 2018-05-17
- Gene:
- FOXD2 NIH gene
- Name:
- forkhead box D2
- Previous symbol:
- FKHL17
- Synonyms:
- FREAC9
- Chromosome:
- 1p33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-18
- Date modifiied:
- 2016-10-05
- Gene:
- IL17A NIH gene
- Name:
- interleukin 17A
- Previous symbol:
- CTLA8, IL17
- Synonyms:
- IL-17A, IL-17
- Chromosome:
- 6p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-25
- Date modifiied:
- 2019-04-23
Related products to: mLST8 (L17) Antigen Human Immunized Animal Rabbit poly IgG, serum Antigen peptide
Related articles to: mLST8 (L17) Antigen Human Immunized Animal Rabbit poly IgG, serum Antigen peptide
- The mechanistic target of rapamycin (mTOR) signaling is influenced by multiple regulatory proteins and post-translational modifications; however, underlying mechanisms remain unclear. Here, we report a novel role of small ubiquitin-like modifier (SUMO) in mTOR complex assembly and activity. By investigating the SUMOylation status of core mTOR components, we observed that the regulatory subunit, GβL (G protein β-subunit-like protein, also known as mLST8), is modified by SUMO1, 2, and 3 isoforms. Using mutagenesis and mass spectrometry, we identified that GβL is SUMOylated at lysine sites K86, K215, K245, K261, and K305. We found that SUMO depletion reduces mTOR-Raptor (regulatory protein associated with mTOR) and mTOR-Rictor (rapamycin-insensitive companion of mTOR) complex formation and diminishes nutrient-induced mTOR signaling. Reconstitution with WT GβL but not SUMOylation-defective KR mutant GβL promotes mTOR signaling in GβL-depleted cells. Taken together, we report for the very first time that SUMO modifies GβL, influences the assembly of mTOR protein complexes, and regulates mTOR activity. - Source: PubMed
Publication date: 2024/02/21
Park Sophia Louise LucilleRamírez-Jarquín Uri NimrodShahani NeelamRivera OscarSharma ManishJoshi Preksha SandipkumarHansalia AayushiDagar SunayanaMcManus Francis PThibault PierreSubramaniam Srinivasa - In addition to their usual use in the treatment of cardiovascular disease, weak evidence is available for the potential of combined use of neprilysin inhibitor (sacubitril) and AT1 receptor antagonist (valsartan) to promote browning of white adipose tissue (WAT) in rats with metabolic syndrome (MetS). This study involved 32 male Wistar albino rats divided into four groups: CTRL-healthy control rats; ENT-healthy rats treated with sacubitril/valsartan; MS-rats with MetS; MS + ENT-rats with MetS treated with sacubitril/valsartan. After finishing the experimental protocol, different WAT depots were isolated for further analysis of molecular pathways. Molecular docking and molecular dynamics studies were used for in silico assessment of the binding affinity of sacubitril and valsartan towards subunits of mechanistic target of rapamycin complex 1 (mTORC1). Sacubitril/valsartan treatment markedly diminished morphological changes in adipose tissue, resulting in smaller lipid size and multilocular lipid droplet structure in WAT. We showed significantly higher protein expression of uncoupling protein-1 (UCP-1) and mTORC1 in WAT of MS + ENT rats, correlating with increased relative gene expression of browning-related markers in tissue of rats treated with sacubitril/valsartan compared with MS group of rats. In silico analysis showed that sacubitrilat and valsartan exhibited the highest binding affinity against mTOR and mLST8, forming stable complexes with these mTORC1 subunits. The observed results confirmed strong potential of combined sacubitril/valsartan treatment to increase browning markers expression in different WAT depots in MetS condition and to form permanent complexes with mTOR and mLST8 subunits over the time. - Source: PubMed
Publication date: 2024/01/29
Nikolic MarinaJeremic NevenaLazarevic NevenaStojanovic AleksandraMilojevic Samanovic AndjelaNovakovic JovanaZivkovic VladimirNikolic MilosNedeljkovic NikolaMitrovic SlobodankaJakovljevic Vladimir - 5-Fluorouracil (5-FU) is currently the main drug used in chemotherapy for gastric cancer (GC). The main clinical problems of 5-FU therapy are insensitivity and acquired resistance to 5-FU. The mechanism of GC cell resistance to 5-FU is currently unknown. - Source: PubMed
Lin XiankePan JiajiaHamoudi HammzaYu Jiren - Idiopathic pulmonary fibrosis (IPF) is considered as a chronic, fibrosing interstitial pneumonia with unknown mechanism. The present work aimed to explore the function, biogenesis and regulatory mechanism of circELP2 in pulmonary fibrosis and evaluate the value of blocking circELP2-medicated signal pathway for IPF treatment. The results showed that heterogeneous nuclear ribonucleoprotein L initiated reverse splicing of circELP2 resulting in the increase of circELP2 generation. The biogenetic circELP2 activated the abnormal proliferation and migration of fibroblast and extracellular matrix deposition to promote pulmonary fibrogenesis. Mechanistic studies demonstrated that cytoplasmic circELP2 sponged miR-630 to increase transcriptional co-activators Yes-associated protein 1 (YAP1) and transcriptional co-activator with PDZ-binding motif (TAZ). Then, YAP1/TAZ bound to the promoter regions of their target genes, such as mTOR, Raptor and mLST8, which in turn activated or inhibited the genes expression in mitochondrial quality control pathway. Finally, the overexpressed circELP2 and miR-630 mimic were packaged into adenovirus vector for spraying into the mice lung to evaluate therapeutic effect of blocking circELP2-miR-630-YAP1/TAZ-mitochondrial quality control pathway in vivo. In conclusion, blocking circELP2-medicated pathway can alleviate pulmonary fibrosis, and circELP2 may be a potential target to treat lung fibrosis. - Source: PubMed
Publication date: 2023/12/30
Zhang SongziTu DiweiLiu WeiliLi RuiqiongJiang MengqiYuan XinglongLuan JianlinLi HongboLv ChangjunSong Xiaodong - The mTOR complexes play a fundamental role in mitochondrial biogenesis and cellular homeostasis. Wat1, an ortholog of mammalian Lst8 is an important component of TOR complex and is essential for the regulation of downstream signaling. Earlier we reported the role of Wat1 in oxidative stress response. Here, we have shown that the abrogation of wat1 causes respiratory defects and mitochondrial depolarization that leads to a decrease in ATP production. The confocal and electron microscopy in wat1Δ cells revealed the fragmented mitochondrial morphology implying its role in mitochondrial fission. Furthermore, we also showed its role in autophagy and the maintenance of calcium ion homeostasis. Additionally, tor2-287 mutant cells also exhibit defects in mitochondrial integrity indicating the TORC1-dependent involvement of Wat1 in the maintenance of mitochondrial homeostasis. The interaction studies of Wat1 and Tor2 with Por1 and Mmm1 proteins revealed a plausible cross-talk between mitochondria and endoplasmic reticulum through the Mitochondria-associated membranes (MAM) and endoplasmic reticulum-mitochondria encounter structure (ERMES) complex, involving TORC1. Taken together, this study demonstrates the involvement of Wat1/mLst8 in harmonizing various mitochondrial functions, redox status, and Ca homeostasis. - Source: PubMed
Publication date: 2023/09/17
Anjum SimmiSrivastava SwatiPanigrahi LalitaAnsari Uzair AhmadTrivedi Arun KumarAhmed Shakil