Rat NT-3 ELISA kit
- Known as:
- Rat NT-3 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- BEK1174
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospect
- Gene target:
- Rat NT-3 ELISA kit
Related genes to: Rat NT-3 ELISA kit
- Gene:
- GCNT4 NIH gene
- Name:
- glucosaminyl (N-acetyl) transferase 4
- Previous symbol:
- LINC01336
- Synonyms:
- C2GNT3
- Chromosome:
- 5q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-06
- Date modifiied:
- 2018-10-18
- Gene:
- INTS3 NIH gene
- Name:
- integrator complex subunit 3
- Previous symbol:
- C1orf60
- Synonyms:
- FLJ21919, INT3, SOSS-A
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-13
- Date modifiied:
- 2014-11-19
- Gene:
- NOTCH4 NIH gene
- Name:
- notch receptor 4
- Previous symbol:
- INT3
- Synonyms:
- -
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-04
- Date modifiied:
- 2019-01-03
- Gene:
- NT3 NIH gene
- Name:
- 3'-nucleotidase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- reserved
- Locus Type:
- unknown
- Date approved:
- 1989-02-23
- Date modifiied:
- 2013-03-27
- Gene:
- SLC25A6 NIH gene
- Name:
- solute carrier family 25 member 6
- Previous symbol:
- ANT3
- Synonyms:
- ANT3Y, MGC17525
- Chromosome:
- Xp22.32 and Yp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-08-03
- Date modifiied:
- 2016-02-18
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- Autism spectrum disorder (ASD) is characterized by aberrations in social interaction and communication associated with repetitive behaviors and interests, with strong clinical heterogeneity. Genetic factors play an important role in ASD, but about 75% of ASD cases have an undetermined genetic risk. We extensively investigated an ASD cohort made of 102 families from the Middle Eastern population of Qatar. First, we investigated the copy number variations (CNV) contribution using genome-wide SNP arrays. Next, we employed Next Generation Sequencing (NGS) to identify or inherited variants contributing to the ASD etiology and its associated comorbid conditions in families with complete trios (affected child and the parents). Our analysis revealed 16 CNV regions located in genomic regions implicated in ASD. The analysis of the 88 ASD cases identified 41 genes in 39 ASD subjects with de novo (n = 24) or inherited variants (n = 22). We identified three novel variants in new candidate genes for ASD (, , and ). Also, we have identified 15 variants in genes that were previously implicated in ASD or related neurodevelopmental disorders (, , , , , , , , , , , , , and ). Additionally, we defined eight novel recessive variants (, , , , , and ), four of which were X-linked. Despite the ASD multifactorial etiology that hinders ASD genetic risk discovery, the number of identified novel or known putative ASD genetic variants was appreciable. Nevertheless, this study represents the first comprehensive characterization of ASD genetic risk in Qatar's Middle Eastern population. - Source: PubMed
Publication date: 2024/03/20
Al-Sarraj YasserTaha Rowaida ZAl-Dous EmanAhram DinaAbbasi SomayyehAbuazab EmanShaath HibahHabbab WesalErrafii KhaoulaBejaoui YosraAlMotawa MaryamKhattab NamatAqel Yasmin AbuShalaby Karim EAl-Ansari AminaKambouris MariosAbouzohri AdelGhazal ImanTolfat MohammedAlshaban FouadEl-Shanti HatemAlbagha Omar M E - Feeding a Saccharomyces cerevisiae fermentation product (SCFP; NutriTek, Diamond V, Cedar Rapids, IA) during periods of metabolic stress is beneficial to the health of dairy cows partially through its effect on the gut microbiota. Whether SCFP alters the ileal microbiota in lactating cows during intestinal challenges induced by feed restriction (FR) is not known. We used 16S rRNA sequencing to assess if feeding SCFP during FR to induce gut barrier dysfunction alters microbiota profiles in the ileum. The mRNA abundance of key genes associated with tissue structures and immunity was also detected. Multiparous cows (97.1 ± 7.6 days in milk (DIM); n = 7 per treatment) fed a control diet or the control plus 19 g/d NutriTek for 9 wk were subjected to an FR challenge for 5 d, during which they were fed 40% of their ad libitum intake from the 7 d before FR. All cows were slaughtered at the end of FR. DNA extracted from ileal digesta was subjected to PacBio Full-Length 16S rRNA gene sequencing. High-quality amplicon sequence analyses were performed with Targeted Amplicon Diversity Analysis and MicrobiomeAnalyst. Functional analysis was performed and analyzed using PICRUSt and STAMP. Feeding SCFP did not (P > 0.05) alter dry matter intake, milk yield, or milk components during FR. In addition, SCFP supplementation tended (P = 0.07) to increase the relative abundance of Proteobacteria and Bifidobacterium animalis. Compared with controls, feeding SCFP increased the relative abundance of Lactobacillales (P = 0.03). Gluconokinase, oligosaccharide reducing-end xylanase, and 3-hydroxy acid dehydrogenase were among the enzymes overrepresented (P < 0.05) in response to feeding SCFP. Cows fed SCFP had a lower representation of adenosylcobalamin biosynthesis I (early cobalt insertion) and pyrimidine deoxyribonucleotides de novo biosynthesis III (P < 0.05). Subsets of the Firmicutes genus, Bacteroidota phylum, and Treponema genus were correlated with the mRNA abundance of genes associated with ileal integrity (GCNT3, GALNT5, B3GNT3, FN1, ITGA2, LAMB2) and inflammation (AOX1, GPX8, CXCL12, CXCL14, CCL4, SAA3). Our data indicated that the moderate FR induced dysfunction of the ileal microbiome, but feeding SCFP increased the abundance of some beneficial gut probiotic bacteria and other species related to tissue structures and immunity. - Source: PubMed
Jiang QianmingSherlock Danielle NElolimy Ahmed AVailati-Riboni MarioYoon IlkyuLoor Juan J - Stressors such as lack of access to feed, hot temperatures, transportation, and pen changes can cause impairment of ruminal and intestinal barrier function, also known as "leaky gut". Despite the known benefits of some nutritional approaches during periods of stress, little is understood regarding the underlying mechanisms, especially in dairy cows. We evaluated the effect of feeding a Saccharomyces cerevisiae fermentation product (SCFP; NutriTek, Diamond V, Cedar Rapids, IA) on the ileal transcriptome in response to feed restriction (FR), an established model to induce intestinal barrier dysfunction. Multiparous cows [97.1 ± 7.6 days in milk (DIM); n = 5/group] fed a control diet or control plus 19 g/d SCFP for 9 wk were subjected to an FR challenge for 5 d during which they were fed 40% of their ad libitum intake from the 7 d before FR. All cows were slaughtered at the end of FR, and ileal scrapping RNA was used for RNAseq (NovaSeq 6000, 100 bp read length). Statistical analysis was performed in R and bioinformatics using the KEGG (Kyoto Encyclopedia of Genes and Genomes) and GO databases. One thousand six hundred and ninety-six differentially expressed genes (DEG; FDR-adjusted P ≤ 0.10) were detected in SCFP vs. control, with 451 upregulated and 1,245 downregulated. "Mucin type O-glycan biosynthesis" was the top downregulated KEGG pathway due to downregulation of genes catalyzing glycosylation of mucins (GCNT3, GALNT5, B3GNT3, GALNT18, and GALNT14). An overall downregulation of cell and tissue structure genes (e.g., extracellular matrix proteins) associated with collagen (COL6A1, COL1A1, COL4A1, COL1A2, and COL6A2), laminin (LAMB2), and integrins (ITGA8, ITGA2, and ITGA5) also were detected with SCFP. A subset of DEG enriched in the GO term "extracellular exosome" and "extracellular space". Chemokines within "Cytokine-cytokine receptor interaction pathways" such as CCL16, CCL21, CCL14, CXCL12, and CXCL14 were downregulated by SCFP. The "Glutathione metabolism" pathway was upregulated by SCFP, including GSTA1 and RRM2B among the top upregulated genes, and GSTM1 and GPX8 as top downregulated genes. There were 9 homeobox transcription factors among the top 50 predicted transcription factors using the RNAseq DEG dataset, underscoring the importance of cell differentiation as a potential target of dietary SCFP. Taken together, SCFP downregulated immune-, ECM-, and mucin synthesis-related genes during FR. Homeobox transcription factors appear important for the transcriptional response of SCFP. - Source: PubMed
Jiang QianmingPalombo ValentinoSherlock Danielle NVailati-Riboni MarioD'Andrea MariasilviaYoon IlkyuLoor Juan J - Metastasis of liver cancer (LC) is the main cause of its high mortality. ETV4 is a critical regulatory factor in promoting LC progression, but the mechanism that ETV4 impacts LC proliferation, migration, and invasion is poorly understood. - Source: PubMed
Publication date: 2023/07/31
Zhou ZhongchengWu BinChen JingShen YiyuWang JingChen XujianFei FamingLi Liang - Pancreatic ductal adenocarcinoma (PDAC) remains a highly fatal malignancy partially due to the acquired alterations related to aberrant protein glycosylation that pathologically remodel molecular biological processes and protect PDAC cells from death. Ferroptosis driven by lethal lipid peroxidation provides a targetable vulnerability for PDAC. However, the crosstalk between glycosylation and ferroptosis remains unclear. Here, we identified 4F2hc, a subunit of the glutamate-cystine antiporter system X, and its asparagine (N)-glycosylation is involved in PDAC ferroptosis by N- and O-linked glycoproteomics. Knockdown of SLC3A2 (gene name of 4F2hc) or blocking the N-glycosylation of 4F2hc potentiates ferroptosis sensitization of PDAC cells by impairing the activity of system X manifested by a marked decrease in intracellular glutathione. Mechanistically, we found that the glycosyltransferase B3GNT3 catalyzes the glycosylation of 4F2hc, stabilizes the 4F2hc protein, and enhances the interaction between 4F2hc and xCT. Knockout of B3GNT3 or deletion of enzymatically active B3GNT3 sensitizes PDAC cells to ferroptosis. Reconstitution of 4F2hc-deficient cells with wildtype 4F2hc restores ferroptosis resistance while glycosylation-mutated 4F2hc does not. Additionally, upon combination with a ferroptosis inducer, treatment with the classical N-glycosylation inhibitor tunicamycin (TM) markedly triggers the overactivation of lipid peroxidation and enhances the sensitivity of PDAC cells to ferroptosis. Notably, we confirmed that genetic perturbation of SLC3A2 or combination treatment with TM significantly augments ferroptosis-induced inhibition of orthotopic PDAC. Clinically, high expression of 4F2hc and B3GNT3 contributes to the progression and poor survival of PDAC patients. Collectively, our findings reveal a previously unappreciated function of N-glycosylation of 4F2hc in ferroptosis and suggest that dual targeting the vulnerabilities of N-glycosylation and ferroptosis may be an innovative therapeutic strategy for PDAC. - Source: PubMed
Publication date: 2023/07/21
Ma HengChen XianlongMo ShengweiZhang YueMao XinxinChen JingciLiu YilinTong Wei-MinLu ZhaohuiYu ShuangniChen Jie