SARS Spike
- Known as:
- SARS Spike
- Catalog number:
- ANT-179
- Product Quantity:
- 100µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- SARS Spike
Related genes to: SARS Spike
- Gene:
- SARS NIH gene
- Name:
- seryl-tRNA synthetase
- Previous symbol:
- -
- Synonyms:
- SERS
- Chromosome:
- 1p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-06-09
- Date modifiied:
- 2014-11-18
- Gene:
- SARS2 NIH gene
- Name:
- seryl-tRNA synthetase 2, mitochondrial
- Previous symbol:
- SARSM
- Synonyms:
- FLJ20450, mtSerRS, SerRSmt, SARS, SERS, SYS
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-09
- Date modifiied:
- 2016-11-09
Related products to: SARS Spike
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- Early identification of emerging dominant variants of pathogens such as SARS-CoV-2 is important for effective public health responses, yet existing approaches are not feasible for real-time surveillance. Here we introduce DeepCoV (DMS-Empowered Evolution Prediction of CoronaVirus), a deep-learning framework for the dynamic identification of emerging variants with high potential to become prevalent at spatiotemporal resolution. It integrates deep mutational scanning (DMS)-derived mutation phenotypes, evolutionary sequence data and epidemiological surveillance data reflecting human immune pressures. Benchmarked against logistic regression-based methods and representative deep-learning approaches in simulated retrospective surveillance scenarios, DeepCoV accurately forecasts the dominance of recently circulating lineages a month in advance, achieving a 90% reduction in false discovery rate while capturing temporal and geographic dynamics of variant spread and reconstructing their regional prevalence trajectories. It also identified mutational hotspots of Omicron-derived backbones in silico, revealing convergent evolution trends. This provides a scalable framework for timely identification of immune-evasive variants and critical mutations, providing actionable insights. - Source: PubMed
Publication date: 2026/05/27
Yang SijieLuo XiaoweiLuo JiejianJian FanchongCao Yunlong - Long-term cognitive impairment is a recognized sequela of the post-COVID-19 condition (PCC). While it is unclear how acute COVID-19 severity contributes to these lasting deficits, some evidence suggests that critical illness may lead to cognitive deficits similar to post-intensive care syndrome. This study examined long-term cognitive, mental, and physical health in patients with varying acute COVID-19 severity (mild to critical), alongside patients critically ill from non-COVID-19 causes. We conducted a bicentric prospective observational study comparing patients with PCC after mild COVID-19 (n = 30), those requiring ICU care for acute COVID-19 (n = 14), and patients with prolonged non-COVID-19 ICU stays (n = 7), all assessed ≥ 12 weeks post-onset. Comprehensive neuropsychological assessments were conducted alongside evaluations of physical impairments, psychiatric symptoms, fatigue and health-related quality of life. Overall cognition was comparable between the mild COVID-19 and ICU groups. However, the mild COVID-19 group experienced higher cognitive fatigue and lower memory satisfaction than both ICU groups, along with higher rates of anxiety (59% vs. 15%) and depression (38% vs. 15%), and reduced mental health-related quality of life compared to COV-ICU patients. Long-term cognitive impairment occurred in PCC patients and ICU survivors, irrespective of acute disease severity. Patients with mild COVID-19 reported greater long-term psychological distress.Trial registration: This study was retrospectively registered at the German Clinical Trials Register, DRKS00025523 on 21 June 2021 ( https://drks.de/search/de/trial/DRKS00025523 ). - Source: PubMed
Publication date: 2026/05/27
Raeder VanessaQuitschau AnnekeGorsler AnnaKülzow NadineSchroeder MariaPohrt AnneEckert IrinaFranke Christiana - SARS-CoV-2 infection affects multiple immune mechanisms and leads to severe COVID-19 and death, in part related to infection-induced or pre-existing autoantibodies. Here, we describe severe COVID-19 to associate with autoantibodies against interleukin-1 receptor antagonist (IL-1Ra) and progranulin (PGRN), endogenous antagonists of IL-1 and TNF signaling, respectively. These autoantibodies coincide with hyperphosphorylation of IL-1Ra (Thr111) or PGRN (Ser81), form immune complexes independent of phosphorylation, reduce antigen plasma levels, and permit enhanced IL-1 and TNF signaling. Using phage-display selected Fabs specific for hyperphosphorylated isoforms, we track phospho-antigens and autoantibodies in a German national pandemic network cohort. Most seropositive patients show both autoantibodies. Levels peak at baseline and decline over 12 months, with phospho-antigens decreasing before autoantibodies. Seropositivity associates with hyperinflammation and cytokine profiles. Importantly, signaling by key inflammatory cytokines induce IL-1Ra and PGRN hyperphosphorylation in healthy monocytes, but require up to 1000-fold higher doses than in monocytes from previously seropositive severe COVID-19 survivors. - Source: PubMed
Publication date: 2026/05/27
Thurner LorenzFadle NatalieThurner BernhardKos Igor AgeBewarder MoritzRegitz EviBette BirgitFischer YvanLesan VadimRixecker TorbenHoffmann Marie-ChristinPreuss Klaus-DieterSchormann ClaudiaKaddu-Mulindwa DominicRoemer KlausCetin OnurMang SebastianBecker AndréSeiler FrederikHerr ChristianLensch ChristianLehmann JohannesThiel-Bodenstaff AngelaLink AndreasWerner ChristianWuchter PatrickKörper SixtenPfuhl ThorstenLohse StefanRissland JürgenThieser KatrinPilch JanPapan CihanRoth SophieVehreschild J JanneScherer MargareteBröhl IsabelWagner PatriciaWitzenrath MartinThibeault CharlotteHaack Ira AnMitrov LazarPütz Sina MReese Jens-PeterKrawczak MichaelHamelmann EckardKopfnagel VerenaFiedler KarinGeisler RamsiaValentin HeikeStahl DanaHanß SabineAmeling SabineVölker UweHansch StefanDörr MarcusBlaschke SabineBraunsteiner JosephineDahl EdgarPape DanielPetersmann AstridStilgenbauer StephanBloos FrankSchrezenmeier HubertLanger FrankGäbelein GereonFriesenhahn-Ochs BettinaPfeifer JochenBauer MichaelBecker Sören LeifNeumann FrankBöhm MichaelAnton GabrieleKuenne CarstenPullamsetti Soni SavaiLooso MarioBals RobertSmola SigrunMeybohm PatrickKrawczyk MarcinLepper Philipp MKessel Christoph - There are no validation studies on patient satisfaction surveys in Spanish that can evaluate a hospital pharmacy drive-thru service. - Source: PubMed
Publication date: 2023/10/21
Romero-Ibarguengoitia Maria ElenaLópez-Zamarrón Katia YackelyneHernández-Treviño Mariana GeorginaGutierrez-González DaliaGonzález-Cantú ArnulfoGonzález Peña Omar IsraelGarza-Silva Arnulfo - SARS-CoV-2 is accountable for severe social and economic disruption around the world causing COVID-19. Non-structural protein-15 (NSP15) possesses a domain that is vital to the viral life cycle and is known as uridylate-specific endoribonuclease (EndoU). This domain binds to the uridine 5'-monophosphate (U5P) so that the protein may carry out its native activity. It is considered a vital drug target to inhibit the growth of the virus. Thus, in this current study, ML-based QSAR and virtual screening of U5P analogues targeting Nsp15 were performed to identify potential molecules against SARS-CoV-2. Screening of 816 unique U5P analogues using ML-based QSAR identified 397 compounds ranked on their predicted bioactivity (pIC50). Further, molecular docking and hydrogen bond interaction analysis resulted in the selection of the top three compounds (53309102, 57398422, and 76314921). Molecular dynamics simulation of the most promising compounds showed that two molecules 53309102 and 57398422 acted as potential binders of Nsp15. The compound was able to inhibit nsp15 activity as it was successfully bound to the active site of the nsp15 protein. This was achieved by the formation of relevant contacts with enzymatically critical amino acid residues (His235, His250, and Lys290). Principal component analysis and free energy landscape studies showed stable complex formation while MM/GBSA calculation showed lower binding energies for 53309102 (ΔG = -29.4 kcal/mol) and 57398422 (ΔG = -39.4 kcal/mol) compared to the control U5P (ΔG = -18.8 kcal/mol). This study aimed to identify analogues of U5P inhibiting the NSP15 function that potentially could be used for treating COVID-19. - Source: PubMed
Publication date: 2023/12/10
Alshahrani Mohammed Merae