Single Licensed Software Package for data logging and computer controlled temperature setting, including a RS 232 Cable
- Known as:
- Single Licensed Software Package data logging and computer controlled temperature setting, including a RS 232 Cable
- Catalog number:
- MD-PCSW-R
- Category:
- -
- Supplier:
- Cleaver
- Gene target:
- Single Licensed Software Package for data logging and computer controlled temperature setting including 232 Cable
Related genes to: Single Licensed Software Package for data logging and computer controlled temperature setting, including a RS 232 Cable
- Gene:
- RUBCN NIH gene
- Name:
- rubicon autophagy regulator
- Previous symbol:
- KIAA0226
- Synonyms:
- rubicon, rundataxin
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-21
- Date modifiied:
- 2019-04-23
Related products to: Single Licensed Software Package for data logging and computer controlled temperature setting, including a RS 232 Cable
"Fish_tail" soft stirring disc for 0.4, 1, 3 and 7l reactor"Fish_tail" soft stirring disc for 0.4, 1, 3 and 7l reactor, modified geometry and material for softer stirring"Two-in-One Image Scanner for Microscope Slides, Filmstrips/Film Slides
Specifically designed for converting microscope slides and films/film slides into digital data formats with high resolution"'Enduroä PAGE 2D System, includes 2D insert and PAGE System components'Enduroä PAGE Electroblotting System, includes the blotting insert and PAGE system components'VX-200 Vortex Mixer Optional head attachment for 24 x 1.5/2.0 ml tubes, 24 x 0.5 ml tubes and 32 x 0.2 ml tubes (or 4 tube strips)'VX-200 Vortex Mixer Optional head attachment for 8 x 15 ml and 8 x 12/13 mm diameter tubes(10) Base holders and cases(1’S,2'S)-Nicotine 1'-Oxide and (1’R,2'S)-Nicotine 1'-Oxide Mixture C10H14N2O CAS:(1’S,2'S)-Nicotine 1'-Oxide and (1’R,2'S)-Nicotine 1'-Oxide Mixture CAS: Formula: C10H14N2O(5) Base holders and cases
(5HCG-HCG ELISA, Fertility and pregnancy(for isolation and cultivation of Listeria from Henry’s light.)(I) LightCycler 1. 0; (Internal Control can't be used for this system) ; (II) LightCycler2. 0; (III) PE5700, MJ_Opticon etc. single color systems; (IV) ABI7000, ABI7300, ABI7500, ABI7900, ABI StepO(Reticular) Fibroblasts and Fibre (human, mouse) - Clone ER-TR7 Related articles to: Single Licensed Software Package for data logging and computer controlled temperature setting, including a RS 232 Cable
- Drug resistance limits the long-term survival of patients with multiple myeloma. The role of tRNA-derived fragments (tsRNAs) in bortezomib resistance in myeloma remains unknown. In this study, the most significantly upregulated tsRNA in relapsed/refractory myeloma was screened. RNA interference was used to explore the function of this tsRNA. The mechanism of the tsRNA-mediated resistance was explored by Ago-RIP-sequencing, dual-luciferase reporter assay, and transmission electron microscopy. tRF-17-8SPOL52 was identified as the most highly expressed tsRNA in relapsed/refractory myeloma. tRF-17-8SPOL52 promoted bortezomib resistance in vitro and in vivo. Ago-RIP-sequencing and dual-luciferase reporter assay showed that tRF-17-8SPOL52 negatively regulated RUBCN. Data from Ago-silenced myeloma cells suggested that the regulation of RUBCN by tRF-17-8SPOL52 was Ago-dependent. Further research showed increased autophagy induced by tRF-17-8SPOL52. In constructed RUBCN overexpressed or inhibited myeloma cells, tRF-17-8SPOL52 promoted cell autophagy by inhibiting RUBCN. Rescue experiments with chloroquine and rapamycin showed that tRF-17-8SPOL52 mediated bortezomib resistance by promoting autophagy. We concluded that tRF-17-8SPOL52 activates autophagy by inhibiting RUBCN in an Ago-dependent manner, which in turn leads to bortezomib resistance in myeloma. - Source: PubMed
Publication date: 2026/08/05
Fu YunfengQiao ZhenrongXiao YulianLiang TingXu Cong - Myocardial ischemia-reperfusion (MIR) injury compromises therapeutic effects of revascularization and leads to functional impairment and exacerbation of structural damage in the heart. Limiting the damage caused by MIR is crucial but is still an unmet clinical need because of the complexity of the underlying mechanisms. Increasing evidence suggests that lysosomal autophagy plays a significant regulatory role in MIR injury. The specific mechanisms involved remain to be fully understood. - Source: PubMed
Publication date: 2026/08/04
Zhou SiyiLiu JiayiHu ManliTian SongZhou JunjieLi WeiChen HailianYin MaojiWang ShiyiLuo LeiZhang LongZhou XiangqiangCheng XuQiu QuanqingWang JinshengQu WeiyiHu YufengFerdinandy PéterChiong MarioTroncoso Mayarling FShan ZhaoliangBai LanYang HailongLiu HuiWan JuanZhang Xiao-JingCai JingjingShe Zhi-GangZhang XinLi Hongliang - Hypoxia-inducible factor 1α (HIF-1α) broadly orchestrates metabolic reprogramming in inflammatory macrophages. However, how HIF-1α shapes the earliest events following activation of pattern recognition receptors and triggers inflammatory responses remain unclear. We found that HIF-1α is functionally active shortly after macrophage inflammatory stimulation via a Rubicon (RUBCN)-NADPH oxidase (NOX2) reactive oxygen species (ROS) circuit, driving glycolysis, cytokine production, and bacterial killing before maximal protein accumulation. Early HIF-1α stabilization primes inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production, which subsequently suppresses electron transport chain function and induces mitochondrial dysfunction independently of RUBCN and NOX2. These findings elucidate a temporally coordinated HIF-1α pathway that integrates RUBCN-NOX2 redox signaling to control macrophage inflammation, metabolic adaptation, and antimicrobial defense. - Source: PubMed
Publication date: 2026/07/21
Davanzo Gustavo GastãoRibeiro GuilhermeDos-Santos DouglasBerçot Marcelo RodriguesZaidan IsabellaMenezes Dos Reis LarissaVirgilio-da-Silva João VictorCastelucci Bianca GazieriEstevão PauloSouza Wanderson DouradoBruneta Henver SFachi José LuisCosta Webster LeonardoAndrade João Nilton BarretoProfeta Gerson SDias Rodrigo RequiãoWassano Natália Sde Brito Monteiro LauarAparecida da Silva Pereira JessicaFavero de Aguiar CristhianeCruz Angelim Monara Kaélle SérvuloSantos Wilias GreisonCarregari Victor CorasollaPeña Jonathande Carvalho Fraga Carlos AlbertoMori Marcelo AConsonni Silvio RobertoMartins-de-Souza DanielVinolo Marco Aurélio RamirezNakaya HelderMurray Peter JBeheshti AfshinCunha Larissa DiasMoraes-Vieira Pedro M - Natural products are biologically active compounds used for therapeutic interventions for various diseases, particularly infections. Autophagy is an intracellular catabolic pathway involving lysosomal degradation and is closely associated with immunological pathways, effectively combating bacterial, viral, fungal, and parasitic infections. Accumulating evidence suggests that autophagy activation or inhibition by natural products promotes antimicrobial responses against various pathogens. Numerous natural products can modulate autophagy through diverse signaling pathways, suggesting their potential as a host-directed therapeutic strategy that may complement conventional drug regimens or help mitigate drug resistance in various infectious diseases. However, it remains largely unclear whether these effects are mediated by direct modulation of autophagy or indirectly through associated mechanisms, including enhanced immune defense, attenuation of pathological inflammation, or crosstalk with other organelle functions. Additionally, multiple pathogens can evade host responses; thus, autophagy activation may inadvertently create favorable conditions for certain pathogens. This review discusses the current knowledge of natural products in terms of their antimicrobial actions through autophagy regulation, particularly the roles of distinct natural product classes, such as polyphenols, alkaloids, terpenoids, quinones, peptides, and macrolides in modulating autophagy for potentially contributing to control various infectious diseases. Exploring the intricate molecular interplay between natural products and autophagy in limiting infections may provide valuable insights that could inform the development of innovative host-directed antimicrobial treatments based on autophagy regulation. 3-MA: 3-methyladenine; AM: alveolar macrophages; AMP: antimicrobial peptides; AMPK: 5' adenosine monophosphate-activated protein kinase; ARDS: acute respiratory distress syndrome; ART: artemisinin; ASFV: African swine fever virus; ATG: autophagy related; AZM: azithromycin; BafA1: bafilomycin A; BECN1: beclin 1; BMDM: bone marrow-derived macrophage; BNIP3: BCL2 interacting protein 3; BNIP3L: BCL2 interacting protein 3 like; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CAMKK2: calcium/calmodulin-dependent protein kinase kinase 2; CBD: cannabidiol; CF: cystic fibrosis; CGA: chlorogenic acid; CGAS: cyclic GMP-AMP synthase; CHUK/IKKα: component of inhibitor of nuclear factor kappa B kinase complex; CLP: cecal ligation and puncture; CLR: clarithromycin; CMA: chaperone-mediated autophagy; CoV: coronavirus; DHT: dihydrotanshinone I; EGCG: epigallocatechin-3-gallate; EIF2A: eukaryotic translation initiation factor 2A; EIF2AK2: eukaryotic translation initiation factor 2 alpha kinase 2; ESKAPE: , and spp.; ESRRA: estrogen related receptor alpha; FOXO1: forkhead box O1; FUNDC1: FUN14 domain containing 1; HBV: hepatitis B virus; HCV: hepatitis C virus; HDT: host-directed therapy; HIV: human immunodeficiency virus; HMGB1: high mobility group box 1; HSV: herpes simplex virus; IAV: influenza A virus; ICT: isocryptotanshinone; IFN: interferon; IKBKB/IKKβ: inhibitor of nuclear factor kappa B kinase subunit beta; IL: interleukin; INH: isoniazid; IRF3: IFN regulatory factor 3; KEAP1: kelch like ECH associated protein 1; LAMP: lysosomal associated membrane protein; LAP: LC3-associated phagocytosis; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPK: mitogen-activated protein kinase; MDM: monocyte-derived macrophage; MDR: multidrug-resistant; MON: monotropein; Mtb: ; MTOR: mechanistic target of rapamycin kinase; mtROS: mitochondrial ROS; NET: neutrophil extracellular trap; NFE2L2/Nrf2: NFE2 like bZIP transcription factor 2; NFKB/NF-κB: nuclear factor kappa B; NLRP3: NLR family pyrin domain containing 3; NLRX1: NLR family member X1; NOTCH1: notch receptor 1; NTM: nontuberculous mycobacteria; OMS: ohmyungsamycin; PAK1: p21 (RAC1) activated kinase 1; PINK1: PTEN induced kinase 1; PKM/PKM2: pyruvate kinase M1/2; PLD: phospholipase D; PM: peritoneal macrophage; PPM1A: protein phosphatase, Mg2+/Mn2+ dependent 1A; PRKN/parkin: parkin RBR E3 ubiquitin protein ligase; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PTEN: phosphatase and tensin homolog; RB1CC1/FIP200: RB1 inducible coiled-coil 1; RELA/p65: RELA proto-oncogene, NF-kB subunit; RIF: rifampicin; ROS: reactive oxygen species; RSV: resveratrol; RUBCN/rubicon: rubicon autophagy regulator; SAR: selective autophagy receptor; SIRT: sirtuin; STING1: stimulator of interferon response cGAMP interactor 1; STX17: syntaxin 17; Tat: trans-activator of transcription; TB: tuberculosis; TBK1: TANK binding kinase 1; TFEB: transcription factor EB; TLR: toll like receptor; TNA: tanshinone IIA; TNF: tumor necrosis factor; UA: ursolic acid; ULK1/Atg1: unc-51 like autophagy activating kinase 1; UPR: unfolded protein response; UVRAG: UV radiation resistance associated; VAMP8: vesicle associated membrane protein 8; VDR: vitamin D receptor; WIPI2: WD repeat domain, phosphoinositide interacting 2; ZFYVE1/DFCP1: zinc finger FYVE-type containing 1; ZIKV: Zika virus. - Source: PubMed
Publication date: 2026/04/28
Paik SeungwhaUm SoohyunKim In SooPark Eun-JinKim Kyung TaeBasu JoyotiOh Dong-ChanJo Eun-Kyeong - Traumatic brain injury (TBI) elicits robust neuroinflammation and oxidative stress, coupled with an acute inhibition of macro-autophagy (autophagy) in neurons and microglia. Rubicon (), a Beclin1 interacting protein that suppresses autophagy and mediates LC3-associated phagocytosis and endocytosis (LAP/LANDO), influences inflammatory signaling in metabolic, neurodegenerative, and inflammaging diseases; yet its role in acquired brain injury has not been defined. Using a controlled cortical impact model, we investigated the role of Rubicon in acute neuroinflammatory responses following injury by comparing wild-type and -mutant mice. Bulk-RNA sequencing of injured cortex revealed attenuated induction of inflammatory pathways and reduced activation of pro-inflammatory microglial/macrophage phenotype in injured -mutant mice. -mutant mice demonstrated less pronounced inhibition of autophagy during the acute phase of injury. Although the inflammatory differences were transient, Rubicon mutant mice exhibited improved motor coordination and gait stability during recovery. Proteomic analyses revealed the presence of a truncated Rubicon protein in the mutant mice and identified the negative regulator of reactive oxygen species (NRROS) as a novel interactor of Rubicon. Consistent with this interaction, -mutant mice displayed markedly reduced oxidative damage, indicated by decreased lipid peroxidation after injury. Together, these findings indicate that Rubicon promotes acute neuroinflammatory and oxidative stress responses following TBI by modulating autophagy and ROS production. Rubicon mediated pathways may serve as therapeutic targets that offer a neuroprotective strategy to improve outcomes after TBI. - Source: PubMed
Publication date: 2026/03/06
Thapa SagarinaMehrabani-Tabari AmirPettyjohn-Robin OliviaNguyen Dexter PhWeldemariam Mehari MSarkar ChinmoyKhan MaryamKane Maureen ALipinski Marta M