Fab'2_ IgG (gamma) hum
- Known as:
- Fab'2_ Immunoglobulin G (g) hum
- Catalog number:
- BI 2504
- Product Quantity:
- 1ml
- Category:
- -
- Supplier:
- P.A.R.I.S
- Gene target:
- Fab'2_ IgG (gamma) hum
Related genes to: Fab'2_ IgG (gamma) hum
- Gene:
- AGPAT3 NIH gene
- Name:
- 1-acylglycerol-3-phosphate O-acyltransferase 3
- Previous symbol:
- -
- Synonyms:
- LPAAT-gamma, LPAAT3
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-16
- Date modifiied:
- 2019-03-26
- Gene:
- AKT3 NIH gene
- Name:
- AKT serine/threonine kinase 3
- Previous symbol:
- -
- Synonyms:
- PKBG, RAC-gamma, PRKBG
- Chromosome:
- 1q43-q44
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-16
- Date modifiied:
- 2018-02-13
- Gene:
- AP1AR NIH gene
- Name:
- adaptor related protein complex 1 associated regulatory protein
- Previous symbol:
- C4orf16
- Synonyms:
- PRO0971, 2C18, gamma-BAR
- Chromosome:
- 4q25
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-15
- Date modifiied:
- 2015-12-17
- Gene:
- BBOX1 NIH gene
- Name:
- gamma-butyrobetaine hydroxylase 1
- Previous symbol:
- BBOX
- Synonyms:
- gamma-BBH, G-BBH, BBH
- Chromosome:
- 11p14.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-26
- Date modifiied:
- 2016-10-05
- Gene:
- CBX3 NIH gene
- Name:
- chromobox 3
- Previous symbol:
- -
- Synonyms:
- HP1Hs-gamma
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-12
- Date modifiied:
- 2015-11-24
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- Genome sequencing (GS) presents a powerful approach to uncover disease-causing genetic variants. We used GS to examine single vs dual molecular causes in some of the most complicated pediatric cases-those with both a neoplasm and a birth defect. - Source: PubMed
Publication date: 2026/01/22
Watson Deborah JSaeidian Amir HosseinWang XiangHarr Margaret HLiu YichuanLi Yun RoseTerek Shannonde Barcelos Isabella PeixotoNesbitt AddieNguyen KennyChang XiaoConnolly JohnHou CuipingSlaby IsabellaWang FengxiangSnyder JamesQiu HaijunQu HuiqiMarch Michael EZhao XiaonanMentch FrankSleiman PatrickGlessner JosephHakonarson Hakon - Lung cancer pathogenesis involves complex interactions between immune system components and metabolic pathways. However, the causal relationships between these factors remain unclear. This study aimed to employ Mendelian randomization (MR) analysis to establish causal links between immunological markers, metabolic factors, and lung cancer development, while integrating multi-omics data for comprehensive molecular characterization. - Source: PubMed
Publication date: 2025/07/28
Yang DunpengZhang WentianWang Qibin - A major challenge in therapeutic approaches applying hematopoietic stem cells (HSCs) is the cell quantity. The primary objective of this study was to predict the miRNAs and anti-miRNAs using bioinformatics tools and investigate their effects on the expression levels of key genes predicted in the improvement of proliferation, and the inhibition of differentiation in HSCs isolated from Human umbilical cord blood (HUCB). A network including genes related to the differentiation and proliferation stages of HSCs was constructed by enriching data of text (PubMed) and StemChecker server with KEGG signaling pathways, and was improved using GEO datasets. Bioinformatics tools predicted a profile from miRNAs containing miR-20a-5p, miR-423-5p, and chimeric anti-miRNA constructed from 5'-miR-340/3'-miR-524 for the high-score genes (RB1, SMAD4, STAT1, CALML4, GNG13, and CDKN1A/CDKN1B genes) in the network. The miRNAs and anti-miRNA were transferred into HSCs using polyethylenimine (PEI). The gene expression levels were estimated using the RT-qPCR technique in the PEI + (miRNA/anti-miRNA)-contained cell groups (n = 6). Furthermore, CD markers (90, 16, and 45) were evaluated using flow cytometry. Strong relationships were found between the high-score genes, miRNAs, and chimeric anti-miRNA. The RB1, SMAD4, and STAT1 gene expression levels were decreased by miR-20a-5p (P < 0.05). Additionally, the anti-miRNA increased the gene expression level of GNG13 (P < 0.05), whereas the miR-423-5p decreased the CDKN1A gene expression level (P < 0.01). The cellular count also increased significantly (P < 0.05) but the CD45 differentiation marker did not change in the cell groups. The study revealed the predicted miRNA/anti-miRNA profile expands HSCs isolated from HUCB. While miR-20a-5p suppressed the RB1, SMAD4, and STAT1 genes involved in cellular differentiation, the anti-miRNA promoted the GNG13 gene related to the proliferation process. Notably, the mixed miRNA/anti-miRNA group exhibited the highest cellular expansion. This approach could hold promise for enhancing the cell quantity in HSC therapy. - Source: PubMed
Publication date: 2024/07/05
Elahimanesh MohammadShokri NafisehShabani RonakRahimi MaryamNajafi Mohammad - Tuft cells are a type of rare epithelial cells that have been recently found to utilize taste signal transduction pathways to detect and respond to various noxious stimuli and pathogens, including allergens, bacteria, protists and parasitic helminths. It is, however, not fully understood how many different types of pathogens they can sense or what exact molecular mechanisms they employ to initiate targeted responses. In this study, we found that an anaerobic pathobiont microbe, (), can induce tuft cell proliferation in the proximal colon whereas the microbe's lysate can stimulate these proximal colonic tuft cells to release interleukin-25 (IL-25). Nullification of the and genes that encode the G protein subunit Gγ13 and transient receptor potential ion channel Trpm5, respectively, or application of the Tas2r inhibitor allyl isothiocyanate (AITC), G protein Gβγ subunit inhibitor Gallein or the phospholipase Cβ2 (PLCβ2) inhibitor U73122 reduces -elicited tuft cell proliferation or IL-25 release or both. Furthermore, conditional knockout or knockout diminishes the expression of gasdermins C2, C3 and C4, and concomitantly increases the activated forms of caspases 3, 8 and 9 as well as the number of TUNEL-positive apoptotic cells in the proximal colon. Together, our data suggest that taste signal transduction pathways are not only involved in the detection of infection, but also contribute to helping maintain gasdermin expression and prevent apoptotic cell death in the proximal colon, and these findings provide another strategy to combat infection and sheds light on new roles of taste signaling proteins along with gasdermins in protecting the integrity of the proximal colonic epithelium. - Source: PubMed
Publication date: 2023/10/25
Lei HaoYu DefuXue Yan-BoLi Yi-HongGong Shi-MengPeng Yuan-YuanLiu Kai-FangBuratto DamianoYang YisenZhang Sai-SaiWu MinZhou RuhongHuang Liquan - Temporal transcription profiles of fetal testes with Sertoli cell ablation were examined in 4-day culture using a diphtheria toxin (DT)-dependent cell knockout system in AMH-TRECK transgenic (Tg) mice. RNA analysis revealed that ovarian-specific genes, including Foxl2, were ectopically expressed in DT-treated Tg testis explants initiated at embryonic days 12.5-13.5. FOXL2-positive cells were ectopically observed in two testicular regions: near the testicular surface epithelia and around its adjacent mesonephros. The surface FOXL2-positive cells, together with ectopic expression of Lgr5 and Gng13 (markers of ovarian cords), were derived from the testis epithelia/subepithelia, whereas another FOXL2-positive population was the 3βHSD-negative stroma near the mesonephros. In addition to high expression of Fgfr1/Fgfr2 and heparan sulfate proteoglycan (a reservoir for FGF ligand) in these two sites, exogenous FGF9 additives repressed DT-dependent Foxl2 upregulation in Tg testes. These findings imply retention of Foxl2 inducibility in the surface epithelia and peri-mesonephric stroma of the testicular parenchyma, in which certain paracrine signals, including FGF9 derived from fetal Sertoli cells, repress feminization in these two sites of the early fetal testis. - Source: PubMed
Publication date: 2023/07/17
Imaimatsu KenyaHiramatsu RyujiTomita AyakoItabashi HirotsuguKanai Yoshiakira