Human VEGF165 Protein Vector: HEK293
- Known as:
- Human VEGF165 Protein Vector: HEK293
- Catalog number:
- 10199-HCyH
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human VEGF165 Protein Vector: HEK293
Related genes to: Human VEGF165 Protein Vector: HEK293
- Gene:
- NRP1 NIH gene
- Name:
- neuropilin 1
- Previous symbol:
- -
- Synonyms:
- NRP, VEGF165R, CD304
- Chromosome:
- 10p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2016-10-05
- Gene:
- NRP2 NIH gene
- Name:
- neuropilin 2
- Previous symbol:
- -
- Synonyms:
- VEGF165R2
- Chromosome:
- 2q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2015-09-01
Related products to: Human VEGF165 Protein Vector: HEK293
Related articles to: Human VEGF165 Protein Vector: HEK293
- The nuanced roles of neuropilin (NRP) isoforms, NRP1 and NRP2, have attracted considerable scientific interest regarding cancer progression. Their differential expressions across various cancer types are specific to NRP isoforms which are shown in a cancer type-dependent manner. It accounts for the different mechanisms involved, driven by a co-expression of gene-sets associated with overexpressed or . Their different expressions on tumour-associated macrophages (TAMs) with disparate markers are associated with the heterogenous tumour microenvironment (TME) through their plasticity and pro-tumorigenic activities. - Source: PubMed
Publication date: 2025/03/11
Han Hyun-JeeRubio-Alarcon MarcosAllen ThomasLee SunwooRahman Taufiq - Bolivian Creole cattle populations evolved under low levels of breeding management and, during more than 500 years of natural selection, became adapted to various environments such as the contrasting highland and subtropical environments. Recently, highland Creole cattle were crossbred with Holstein to improve dairy production. The aim of this research was to evaluate the divergent adaptation through selection footprints of Bolivian Creole cattle from Andean highland and tropical lowlands, and to evaluate the effect of Holstein introgression in highland Creole. For this purpose, 130 Creole cattle (75 highland, 55 lowland) and 88 Holstein were genotyped using a microarray. The database was used to determine population structure and admixture and detect selection sweeps using F, Rsb, XP-EHH, and ROH. Ancestry inference suggested that selection peaks were not due to Holstein introgression. The NCBI database was used to retrieve genes from the common regions and then perform gene ontology analysis. The most prominent selection peaks were on BTA20 and BTA23 and included the PRLR (slick phenotype) and Class I and IIa BoLA genes. Other windows contained candidate genes for hypoxia (ANXA2, NDUFA4L2), angiogenesis and haematological parameters (ANXA2, CPLANE1, NRP1, NRP2), immune response (IL7R, IL6ST, IL31RA, C6, C7, STAT6, NKG2A, IRAK4, KLR, CLEC), oxidative stress (GSTA, HSD17B6) and morphological traits (PLAG1, CHCHD7, CAP2, ARL15). GO analysis revealed enrichment terms and pathways related to immune response, glutathione and retinol metabolism and reported QTLs for coat characteristics, immune response and tick resistance. The results suggest the complex mechanism in the adaptation of Bolivian Creole cattle to the contrasting highland and subtropical environments. - Source: PubMed
Publication date: 2025/02/25
Marcuzzi OliviaCecco Paulo ÁlvarezOlivera Leónidas HPereira Rico Juan ACalcaterra FranciscoVega Ariel LozaPeral-García PilarFernández María EMuñoz Andrés RogbergGiovambattista Guillermo - Although Amyloid-beta and Tau are the hallmarks of Alzheimer's Disease (AD), other protein pathways such as endothelial dysfunction may be involved and may precede cognitive symptoms. Our objective was to characterize the cerebrospinal fluid (CSF) proteomic profiles focusing on cardiometabolic-related protein pathways in individuals on the AD spectrum. - Source: PubMed
Publication date: 2025/01/16
Neal ReemYang ZhiyiObideen MalikPeterson MelissaShah AmilHajjar Ihab - Despite all the progress in treating SARS-CoV-2, escape mutants to current therapies remain a constant concern. Promising alternative treatments for current and future coronaviruses are those that limit escape mutants by inhibiting multiple pathogenic targets, analogous to the current strategies for treating HCV and HIV. With increasing popularity and ease of manufacturing of RNA technologies for vaccines and drugs, therapeutic microRNAs represent a promising option. In the present work, miR-24-3p was identified to inhibit SARS-CoV-2 entry, replication, and production; furthermore, this inhibition was retained against common mutations improving SARS-CoV-2 fitness. To determine the mechanism of action, bioinformatic tools were employed, identifying numerous potential effectors promoting infection targeted by miR-24-3p. Of these targets, several key host proteins for priming and facilitating SARS-CoV-2 entry were identified: furin, NRP1, NRP2, and SREBP2. With further experimental analysis, we show that miR-24-3p directly downregulates these viral entry factors to impede infection when producing virions and when infecting the target cell. Furthermore, we compare the findings with coronavirus, HCoV-229E, which relies on different factors strengthening the miR-24-3p mechanism. Taken together, the following work suggests that miR-24-3p could be an avenue to treat current coronaviruses and those likely to emerge. - Source: PubMed
Publication date: 2024/11/28
Evers ParrishUguccioni Spencer MAhmed NadineFrancis Magen EKelvin Alyson APezacki John P - Neutrophil elastase (NE) has been reported to be a pro-inflammatory stimulus for macrophages. The aim of the present study was to determine the impact of NE exposure on the human macrophage proteome and evaluate its impact on pro-inflammatory signals. Human blood monocytes from healthy volunteers were differentiated to macrophages and then exposed to either 500 nM of NE or control vehicle for 2 h in triplicate. Label-free quantitative proteomics analysis identified 41 differentially expressed proteins in the NE versus control vehicle datasets. A total of 26 proteins were downregulated and of those, 21 were cell surface proteins. Importantly, four of the cell surface proteins were proteoglycans: neuropilin 1 (), syndecan 2 (), glypican 4 (), and CD99 antigen-like protein 2 () along with neuropilin 2 (), CD99 antigen (), and endoglin () which are known interactors. Additional NE-targeted proteins related to macrophage function were also measured including , , , , and . Collectively, this study provides a comprehensive unbiased view of selective NE-targeted cell surface proteins in chronically inflamed lungs. - Source: PubMed
Publication date: 2024/12/04
Ahmed Nadia TasnimKummarapurugu Apparao BZheng ShuoBulut GamzeKang LeBatheja AashishHawkridge AdamVoynow Judith A