AZUR II EOSIN, CAS 53092_85_6
- Known as:
- AZUR II EOSIN, CAS 53092_85_6
- Catalog number:
- 1694
- Product Quantity:
- 25 gm
- Category:
- -
- Supplier:
- TitanBiotech
- Gene target:
- AZUR EOSIN CAS 53092_85_6
Related genes to: AZUR II EOSIN, CAS 53092_85_6
- Gene:
- AZU1 NIH gene
- Name:
- azurocidin 1
- Previous symbol:
- -
- Synonyms:
- AZU, CAP37, AZAMP, HBP, NAZC, HUMAZUR
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-21
- Date modifiied:
- 2014-11-18
Related products to: AZUR II EOSIN, CAS 53092_85_6
Paliperidone N-Oxide C23H27FN4O4 CAS: 761460-08-6 Paliperidone N-Oxide CAS: 761460-08-6 Formula: C23H27FN4O4 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3,16α-diol C20H24Br2O4 CAS: 90474-20-7 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3,16α-diol CAS: 90474-20-7 Formula: C20H24Br2O4 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3-ol C20H24Br2O3 CAS: 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3-ol CAS: Formula: C20H24Br2O3 3,3',5,5'-Tetraiodo Thyroformic Acid C13H6I4O4 CAS: 2055-97-2 3,3',5,5'-Tetraiodo Thyroformic Acid CAS: 2055-97-2 Formula: C13H6I4O4 3,5,3',5'-Tetrachlorobisphenol A C15H12Cl4O2 CAS: 79-95-8 3,5,3',5'-Tetrachlorobisphenol A CAS: 79-95-8 Formula: C15H12Cl4O2 4-(2,6,6-Trimethyl-2-cyclohexen-1-ylidene)-2-acetoxybut-2-ene C15H22O2 CAS: 61693-39-8 4-(2,6,6-Trimethyl-2-cyclohexen-1-ylidene)-2-acetoxybut-2-ene CAS: 61693-39-8 Formula: C15H22O2 4-Benzyloxy-1-cyclohexanecarbonitrile (cis / trans mixture) CAS: 95233-32-2 Formula: C14H17NO 4-Benzyloxy-1-cyclohexanecarbonitrile (cis _ trans mixture) C14H17NO CAS: 95233-32-2 5-[(4-Methoxyphenyl)-diphenylmethylamino-6-methoxy-9H-purin-9-yl]-13C2, 15N-3-(phenylmethoxy)-2-[(phenylmethoxy)methyl]-cyclopentanol CAS: Formula: Related articles to: AZUR II EOSIN, CAS 53092_85_6
- Among individuals with neuropsychiatric disorders, those with bipolar disorder (BD) have one of the highest rates of suicide with this risk even further elevated in the Veteran population. The assessment of suicide risk is clinically challenging, but one of the best predictors of a future suicide attempt is having a prior attempt. Although prior studies have implicated proteomic abnormalities separately in BD and among those with a suicide attempt history, little is known regarding their combined contribution to suicide risk in BD and/or their relationship to the brain white matter. - Source: PubMed
Publication date: 2026/05/25
Szeszko Philip RChan Chi CRamakrishnan AarthiRizk MinaBaptista IsabelleAlter SharonHaznedar M MehmetChu King-WaiXie HuiYehuda RachelRusso Scott JShen LiRizakos TiaD'Souza DarwinFleysher LazarHazlett Erin AGoodman MarianneKim-Schulze SeungheeMurrough James W - Extracellular vesicles derived from induced pluripotent stem cells (iPSC EVs) have immunoregulatory potential with the ability to alter the macrophage phenotype. Modulating the macrophage phenotype towards an anti-inflammatory, pro-resolving state may be beneficial in the treatment of chronic inflammatory diseases. The contents of iPSC EVs and their effects on macrophages are poorly understood. Here iPSC EVs were characterized and analysed by mass spectrometry-based proteomics and a targeted microRNA (miR) panel and their immunomodulatory effects on primary human macrophages were assessed. Podocalyxin-like protein 1 (PODXL1) and Insulin (INS) were the most abundant proteins unique to the iPSC EVs while miR-302d-3p was the most abundant miR. Notably, thioredoxin- and peroxiredoxin-related proteins were detected. iPSC EVs increased the anti-inflammatory associated Mannose Receptor C-Type 1 (MRC1) and miR-21, while monocyte chemoattractant protein 1 (MCP-1) and IL-8 were decreased. Proteomics revealed that treated macrophages had decreased levels of chemoattractant proteins, Azurocidin 1 (AZU1), Growth Differentiation Factor 15 (GDF15), and Ribosomal Protein S19 (RPS19). Conditioned media from macrophages treated with iPSC EVs inhibited monocyte transmigration, a key component in the propagation of inflammation. This study provides insights into the protein and miR cargo of iPSC EVs and highlights their capacity to inhibit chemotactic proteins in macrophages. - Source: PubMed
Publication date: 2026/05/09
Fitzsimons StephenOggero SilviaEgan Billy PDillon Eugène TMartín María Muñoz-SanClerkin ShaneKennedy CiaránDavis JessicaAndrews DarrellCrean JohnBelton Orina - Dipeptidyl peptidase-1 (DPP1) inhibitors prevent the activation of neutrophil serine proteases and reduce exacerbations in people with bronchiectasis. We previously identified a novel effect of DPP1 inhibitors in reducing the neutrophil pseudoenzyme azurocidin-1 (AZU1). The aim of this study was to investigate the role of AZU1 in the pathophysiology of bronchiectasis. - Source: PubMed
Publication date: 2026/04/24
Shoemark AmeliaJohnson Emma DShuttleworth MorvenSchwiening MaxHull RebeccaStobo JamieAbo-Leyah HaniFinch SimonPollock JenniferHuang Jeffrey T JRichardson HollianPerea LidiaMcIntosh EveCant ErinGalloway RachelChoi Hayoungde Soyza AnthonySpinou AriettaRingshausen Felix CLorent NatalieMallia PatrickJohnston Sebastian LGierlinski MarekGoeminne PieterLoebinger Michael RHua Gao YongChotirmall Sanjay HDhar RajaHaworth CharlesAltenburg JosjeBlasi FrancescoPolverino EvaShteinberg MichalStrickson SamCipolla DavidTeper ArielFernandez CarlosShih Vivian HMange KevinSinganayagam AranAliberti StefanoSibila OriolLong Merete BChalmers James D - Sepsis-associated acute kidney injury (SA-AKI) is one of the most common and severe complications in clinical practice, with high incidence and mortality rates. This work aimed to demonstrate the predictive value of the inflammatory factors nucleotide-binding oligomerization domain-like receptor protein (NLRP), procalcitonin (PCT), and heparin-binding protein (HBP) for SA-AKI and assess the impact of anti-inflammatory drug therapy on its clinical efficacy. About 120 patients with SA-AKI admitted to our hospital from January 2020 to December 2022 were enrolled, and they were categorized into survival group (82 cases) and death group (38 cases) regarding the outcomes. The levels of NLRP, PCT, and HBP in the blood of both groups were measured, and receiver operating characteristic curves were plotted to evaluate the predictive value of mortality risk factors in SA-AKI patients. The SA-AKI patients received anti-inflammatory drug therapy, and clinical indicators were compared pre- and post-treatment. NLRP, PCT, and HBP in survival group were notably inferior to death group (P < .05). The survival group had greatly inferior acute physiology and chronic health evaluation II scores and sequential organ failure assessment scores to death group (P < .05). NLRP, PCT, and HBP showed positive predictive values for the prognosis of SA-AKI. After anti-inflammatory drug treatment, patients exhibited reduced levels of inflammation, improved renal function, increased urine output, rapid decline in serum creatinine levels, and milder renal injury (P < .05). The anti-inflammatory treatment exhibited a significantly higher overall efficacy rate in patients compared to those for whom the treatment was ineffective (P < .05). NLRP, PCT, and HBP, as inflammatory factors, have high predictive value for the early diagnosis and evaluation of SA-AKI. Anti-inflammatory drug therapy effectively reduces inflammation levels, improves renal function, and mitigates kidney damage in patients. - Source: PubMed
Fang ZhidongCui ShuqinLiu XianShi MinZheng WeiXue JingChen Li - Diabetic kidney disease (DKD) is a severe complication of diabetes mellitus and the leading cause of chronic kidney disease worldwide. Among the many drivers of tubular injury, lipid accumulation and inflammation are emerging as major contributors to kidney disease progression, but the molecular link between lipid metabolism and inflammatory signaling remains to be determined. - Source: PubMed
Publication date: 2026/02/07
Meadows KieranChung HyunjaeVo SonImanzadeh AysaSeo HeewonBelay Sisay GetieSwamy AshaTeo WulinChapman KevinAndonegui GracielaBenediktsson HallgrimurStys Peter KPham ThangMuruve Daniel AChun Justin