Defensin_1 (human) HNP_1 Formula C150H222N44O38S6 Sequence Ala_Cys_Tyr_Cys_Arg_Ile_Pro_Ala_Cys_Ile_Ala_Gly_Glu_Arg_Arg_Tyr_Gly_Thr_Cys_Ile_Tyr_Gln_Gly_Arg_Leu_Trp_Ala_Phe_Cys_Cys(Disulfide bridges C
- Known as:
- Defensin_1 (H. sapiens) HNP_1 Formula C150H222N44O38S6 Sequence Ala_Cys_Tyr_Cys_Arg_Ile_Pro_Ala_Cys_Ile_Ala_Gly_Glu_Arg_Arg_Tyr_Gly_Thr_Cys_Ile_Tyr_Gln_Gly_Arg_Leu_Trp_Ala_Phe_Cys_Cys(Disulfide bridges C
- Catalog number:
- 100512
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- GLSChina
- Gene target:
- Defensin_1 (human) HNP_1 Formula C150H222N44O38S6 Sequence Ala_Cys_Tyr_Cys_Arg_Ile_Pro_Ala_Cys_Ile_Ala_Gly_Glu_Arg_Arg_Tyr_Gly_Thr_Cys_Ile_Tyr_Gln_Gly_Arg_Leu_Trp_Ala_Phe_Cys_Cys(Disulfide bridges
Related products to: Defensin_1 (human) HNP_1 Formula C150H222N44O38S6 Sequence Ala_Cys_Tyr_Cys_Arg_Ile_Pro_Ala_Cys_Ile_Ala_Gly_Glu_Arg_Arg_Tyr_Gly_Thr_Cys_Ile_Tyr_Gln_Gly_Arg_Leu_Trp_Ala_Phe_Cys_Cys(Disulfide bridges C
Paliperidone N-Oxide CAS: 761460-08-6 Formula: C23H27FN4O4 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 CAS: Formula: C20H24Br2O3 3,3',5,5'-Tetraiodo Thyroformic Acid CAS: 2055-97-2 Formula: C13H6I4O4 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 CAS: 61693-39-8 Formula: C15H22O2 4-Benzyloxy-1-cyclohexanecarbonitrile (cis / trans mixture) CAS: 95233-32-2 Formula: C14H17NO 5-[(4-Methoxyphenyl)-diphenylmethylamino-6-methoxy-9H-purin-9-yl]-13C2, 15N-3-(phenylmethoxy)-2-[(phenylmethoxy)methyl]-cyclopentanol CAS: Formula: 6-Phenylhexylamine Hydrochloride CAS: 120375-57-7 Formula: C12H20ClN Paliperidone-d4 CAS: 1020719-55-4 Formula: C23H23D4FN4O3 [Tyr63] PTH (63_84), human
Human ELC ELISA KIT 96 TEST
"Recombinant Human Carboxypeptidase E_CPE""Recombinant Human Carboxypeptidase E_CPE""Recombinant Human Carboxypeptidase E_CPE" Related articles to: Defensin_1 (human) HNP_1 Formula C150H222N44O38S6 Sequence Ala_Cys_Tyr_Cys_Arg_Ile_Pro_Ala_Cys_Ile_Ala_Gly_Glu_Arg_Arg_Tyr_Gly_Thr_Cys_Ile_Tyr_Gln_Gly_Arg_Leu_Trp_Ala_Phe_Cys_Cys(Disulfide bridges C
- Neoadjuvant therapy (NAT) followed by radical surgery is the standard treatment for locally advanced esophageal squamous cell carcinoma (LA-ESCC), yet many patients fail to achieve pathologic complete response (pCR). Predictive biomarkers and biological mechanisms underlying NAT resistance remain elusive. We aimed to address this challenge through longitudinal multi-omics profiling of patient plasma during NAT. - Source: PubMed
Publication date: 2026/07/15
Xiao ChuDeng ZiqinZhang GuochaoYang ZhenlinZhang LongYin HongfeiFan TaoWang DiLiu YixiaoCai WenpengJi YuLi JiaLiao TianleLi ChunxiangHe Jie - To investigate the expression of C-C motif chemokine receptor-like 2 (CCRL2) on platelets in children with chronic primary immune thrombocytopenia(ITP), and its effect on platelet function. - Source: PubMed
Yang FeiWang QiLi YangLu QinGao Yuan-YuanWu Li-XiaShao Xue-Jun - Occupational noise-induced hearing loss (NIHL) is a common occupational disorder, yet non-invasive molecular indicators of chronic occupational noise exposure remain insufficiently characterized. Although the cochlear mechanisms behind NIHL have been extensively studied in experimental models, peripheral blood transcriptomic alterations in affected human populations are less well defined. In this exploratory study, we aimed to describe peripheral blood gene expression patterns associated with occupational NIHL and to generate candidate molecular signals for future validation. Peripheral blood RNA sequencing (RNA-seq) was performed in 11 male individuals with occupational bilateral sensorineural hearing loss and four noise-unexposed healthy male controls. Transcript abundance was quantified using a standardized RNA-seq workflow, and formal differential expression analysis was conducted on gene-level count data derived from Salmon quantification using DESeq2 with Benjamini-Hochberg correction. Through our analysis, we identified a limited set of differentially expressed genes, including upregulated interferon-associated transcripts, such as , , , and , host-defense-related genes, including , , and , and immune-regulatory transcripts such as and , together with downregulated non-coding RNAs including and . These findings suggest that occupational NIHL may be accompanied by detectable peripheral blood transcriptomic alterations, predominantly involving immune- and host-defense-related pathways. Given the limited cohort size and exploratory design, these genes represent preliminary candidates for validation in larger independent cohorts. - Source: PubMed
Publication date: 2026/05/08
Öztan Gözdeİşsever HalimGüldiken YahyaCanbaz SevgiOğuz FatmaKurt Özlem Karİşsever Tuğçe - Acute respiratory exacerbations in bronchiectasis are important as they impair quality of life and are associated with accelerated lung function decline. Yet, no validated methods exist to identify children at increased risk of exacerbations. We therefore determined if peripheral blood gene expression (GE) signatures can identify those at risk of an impending exacerbation. Thirty-one children with bronchiectasis had RNA extracted from peripheral blood collected whilst they were clinically stable, with 22 having an exacerbation during the next 3 months. Microarray assays using the HumanHT-12 v4.0 Expression BeadChip identified differentially expressed genes (p value ≤ 0.05, fold change > 1.5). The top targets were verified using real-time quantitative polymerase chain reaction (rt-qPCR) assays, and receiver operating characteristics and area under the curve (AUC) were assessed. Functional analysis of these genes was performed using Ingenuity Pathway Analysis. Overall, 647 entities were significantly dysregulated (p < 0.05) in the exacerbation group (n = 22), and pathway analysis identified neutrophil degranulation as the dominant affected pathway, which was also significantly inhibited (p < 0.001). Forty entities (32 genes) were associated with a future exacerbation (p ≤ 0.05, fold change ≥ 1.5) and six genes (ANXA3, ALAS2, DEFA1, ALPL, SNCA, PROK2) were verified using RT-qPCR (all p < 0.04) as the most discriminatory. DEFA1 and ANXA3 had the highest AUC (0.92, 95% confidence interval [CI] 0.82-1.00, and 0.87, 95% CI 0.73-1.00, respectively). We identified neutrophil-associated genes from peripheral blood that could be potential biomarkers for children with bronchiectasis at increased risk of exacerbations during the next 3 months. These GE signatures warrant further investigation and validation in larger, independent cohorts. KEY MESSAGES: Exacerbations in paediatric bronchiectasis are important. Peripheral blood gene expression may help identify children at risk of exacerbations. Six neutrophil-associated genes were associated with a future exacerbation. Identifying predictive gene expression signatures warrants further investigation. - Source: PubMed
Publication date: 2026/04/01
O'Farrell Hannah EGoyal VikasChang Anne BGrimwood KeithCheng MichaelYerkovich Stephanie TBaines Katherine J - Intestinal ischemia/reperfusion (I/R) injury presents a biphasic pathology: an acute oxidative-inflammatory phase leading to organ failure, and a recovery phase marked by mucosal dysfunction and bacterial translocation. The developed MPB@TA-Cu-Ma nanocomposite functions as a dual-phase therapeutic platform with significant efficacy. It rapidly scavenges reactive oxygen species (ROS) (exhibiting a 50.15% higher clearance in vitro) and suppresses macrophage pyroptosis within 6 h post-I/R. Furthermore, it enhances mucosal integrity (1.98-fold Occludin upregulation) and angiogenesis (3.6-fold increase in CD31 cells) by 96 h. Transcriptomic and immunohistochemical analyses identify three key mechanisms underlying this efficacy: (1) inhibition of the NOD-like receptor family pyrin domain-containing 3 (NLRP3)/ cysteinyl aspartate-specific proteinase 1 (caspase-1) pathway to suppress pyroptosis; (2) upregulation of defensin alpha 1 (DEFA1) and desmoglein 1 (DSG1) for epithelial repair; and (3) enhancement of vascular endothelial growth factor (VEGF) and angiotensin-converting enzyme (ACE) expression for vascular regeneration. Overall, MPB@TA-Cu-Ma achieves synchronized, phase-adaptive therapy by disrupting the oxidative-inflammatory-barrier axis through enhanced ROS scavenging, enzyme-mimetic activity, promotion of angiogenesis, and immune modulation, thereby effectively addressing the complex biphasic pathology of intestinal I/R injury. - Source: PubMed
Publication date: 2026/03/31
Qiu ChenghaoXian WenjingWang MengxueZhao GuozhiZhang YanhuoZhou ZhiyuSheng BoZhen ZhuoLiu XieDiao ShouwenTu MengweiQiu ChenWang HuixianZhang JianboZhu PengLi Tong