ErbB3 Fragment (ErbB3-f), Human
- Known as:
- ErbB3 Fragment (ErbB3-f), Human
- Catalog number:
- Z02748-20
- Product Quantity:
- 20,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- ErbB3 Fragment (ErbB3-) Human
Related genes to: ErbB3 Fragment (ErbB3-f), Human
- Gene:
- ERBB3 NIH gene
- Name:
- erb-b2 receptor tyrosine kinase 3
- Previous symbol:
- LCCS2
- Synonyms:
- HER3
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-15
- Date modifiied:
- 2019-04-23
Related products to: ErbB3 Fragment (ErbB3-f), Human
Related articles to: ErbB3 Fragment (ErbB3-f), Human
- The Kazakh mare, an indigenous breed of Xinjiang, exhibits strong adaptability to arid and cold conditions while maintaining relatively stable milk production under low-input extensive farming systems. However, its genetic improvement has been constrained by traditional management practices. - Source: PubMed
Publication date: 2026/07/06
Meng ChenLuo PenghuiRen WanluXie XiaoyuZeng YaqiWang JianwenYao XinkuiMeng Jun - The Belgian Precision initiative aims to implement tumor-agnostic next-generation sequencing (NGS) in patients with advanced cancer and expand genotype-matching drug availability. The present investigator-driven trial aimed to study the efficacy of afatinib in patients with advanced solid tumors harboring an activating HER2, EGFR, or HER3 mutation. - Source: PubMed
Publication date: 2026/07/06
Decoster LoreAftimos PhilippeRottey SylviePrenen HansCollignon JoelleMebis JeroenCanon Jean LucFastenaekels VanessaCappoen NadiaKondrat AnnaJoris SofieDe Grève Jacques - Gastric-type endocervical adenocarcinoma (G-EAC) is a rare, highly aggressive malignancy that is not associated with human papillomavirus (HPV) infection. Its occurrence in patients with Peutz-Jeghers syndrome (PJS) is exceptionally rare but clinically critical. In this preliminary study, we performed comprehensive genomic profiling (CGP) using a targeted next-generation sequencing (NGS) panel and immunohistochemistry (IHC) for key biomarkers on a single, well-characterized patient with stage IB3 PJS-associated G-EAC. The primary objective was to identify actionable genomic alterations and potential therapeutic targets to inform personalized treatment strategies. CGP revealed a pathogenic germline p.K84* mutation, alongside somatic p.G12A and p.R667S mutations. IHC demonstrated strong, diffuse positivity for Claudin18.2 and MUC6, confirming a gastric phenotype, while p16 was negative. The integration of genomic and proteomic data revealed a primary actionable target, Claudin18.2 (a proven target in gastric cancer), alongside potential actionable alterations involving ERBB signaling. This proof-of-concept study may suggest that integrating CGP and IHC in the management of PJS-associated G-EAC is feasible and could potentially inform clinical decision-making. The identification of these targets could suggest a rationale for incorporating molecular profiling into the standard diagnostic workflow for this aggressive malignancy, potentially improving outcomes through precision oncology approaches. - Source: PubMed
Publication date: 2026/06/18
Niu TianhuiLiu XiaofangZhang SiqiYu MengnanWang XiaoyingJia Jinghui - This study aims to investigate the effect of modified Xiangsha Liujunzi Decoction on adipose tissue browning-neuregulin 4(Nrg4)-liver fatty acid synthesis pathway in the rat model of both spleen deficiency and hyperlipidemia. Seventy SPF-grade male SD rats were randomly assigned into blank control(CON), high-fat diet(HFD), spleen deficiency and high-fat diet(SD-HFD), rosuvastatin(RSF), low-, medium-, and high-dose modified Xiangsha Liujunzi Decoction(XS-L, XS-M, and XS-H, respectively) groups, with 10 rats in each group. The rats in the SD-HFD, RSF, XS-L, XS-M, and XS-H groups were modeled for spleen deficiency by an improper diet combined with swimming exhaustion for a total of 15 days. The CON group was fed with a normal diet while the other groups with a high-fat diet for 10 weeks after successful modeling of spleen deficiency. The RSF, XS-L, XS-M, and XS-H groups were administrated with corresponding drugs by gavage for 8 weeks and the other groups were administrated with an equal volume of distilled water. The feeding method of each group was kept unchanged during the period of gavage. Four items of serum lipids were measured by an automatic biochemical analyzer. The pathological changes in the interscapular brown adipose tissue(BAT), abdominal white adipose tissue(WAT), and liver were observed by hematoxylin-eosin(HE) staining. The liver lipid deposition was observed by oil red O staining and the serum Nrg4 level was measured by enzyme-linked immunosorbent assay(ELISA). RT-qPCR was employed to determine the mRNA levels of peroxisome proliferator-activated receptor gamma(PPARγ), peroxisome proliferator-activated receptor gamma cofactor 1α(PGC1α), uncoupling protein 1(UCP1), and Nrg4 in the adipose tissue and liver X receptor alpha(LXRα), sterol regulatory element-binding protein-1c(SREBP-1c), acetyl-CoA carboxylase(ACC), and stearoyl-CoA desaturase 1(SCD1) in the liver tissue of rats in each group. Western blot was employed to quantify the protein levels of PPARγ, PGC1α, UCP1, and Nrg4 in the adipose tissue and Erb-B2 receptor tyrosine kinase 3(ErbB3), phosphorylated ErbB3(p-ErbB3), Erb-B2 receptor tyrosine kinase 4(ErbB4), phosphorylated ErbB4(p-ErbB4), signal transducer and activator of transcription 5(STAT5), phosphorylated STAT5(p-STAT5), LXRα, SREBP-1c, ACC, and SCD1 in the liver tissue. Compared with the CON group, the HFD and SD-HFD groups showed significantly elevated serum levels of triglycerides(TG), total cholesterol(TC), high-density lipoprotein-cholesterol(HDL-C), and low-density lipoprotein-cholesterol(LDL-C) and a significantly declined level of Nrg4. HE staining revealed enlarged BAT and WAT cells and increased lipid vacuoles in hepatocytes in the HFD and SD-HFD groups. The oil red O staining showed that the HFD and SD-HFD groups had more orange lipid droplets in hepatocytes than the CON group. Compared with the CON group, the SD-HFD group showed significantly down-regulated mRNA and protein levels of PPARγ, PGC1α, and Nrg4, significantly down-regulated protein levels of UCP1 in both BAT and WAT cells, and a significantly down-regulated mRNA level of UCP1 in BAT cells. In addition, the SD-HFD group showed significantly decreased p-ErbB3/ErbB3, p-ErbB4/ErbB4, and p-STAT5/STAT5 ratios and significantly up-regulated mRNA and protein levels of LXRα, SREBP-1c, ACC, and SCD1 in the liver tissue. Compared with the SD-HFD group, the RSF, XS-M, and XS-H groups showed significantly declined serum TG, TC, and LDL-C levels, and the XS-M and XS-H groups presented significantly elevated serum Nrg4 levels. In addition, these groups showed reductions in volumes of BAT and WAT cells, alleviated hepatocyte swelling, and decreased lipid droplets in hepatocytes. The mRNA and protein levels of related factors were improved in XS-M and XS-H groups compared with those in the SD-HFD group. This study indicates that modified Xiangsha Liujunzi Decoction could promote the browning of adipose tissue, increase the expression of Nrg4 in the adipose tissue, raise the level of circulating Nrg4, and reduce liver fatty acid synthesis in the rat model of both spleen deficiency and hyperlipidemia. - Source: PubMed
Qiao AiZhao NaZhang QiChe Meng-ZhuSui Guo-YuanJia Lian-Qun - Increasing evidence supports associations between cognitive function and autoimmune disorders, yet the underlying genetic mechanisms remain unclear. Using large-scale genome-wide association statistics for seven cognitive traits and fifteen autoimmune disorders, together with two independent cohorts comprising 522 healthy individuals and 80 patients with schizophrenia, we performed multi-level pleiotropic analyses. Genetic correlation analyses identified nine significant cognition-immune linkage pairs, whereas Mendelian randomization (MR) analyses suggested that these associations were largely driven by shared genetic architecture rather than causality. Using PLACO, colocalization analysis, and MAGMA analyses, we identified 46 pleiotropic loci and 169 pleiotropic genes across the linkage pairs. Polygenic risk scores derived from pleiotropic variants were associated with cognition in healthy adults and showed nominal associations in schizophrenia. Enrichment analyses linked these genes to cognition-immune-related tissues, pathways, and biological processes, while multi-trait colocalization highlighted CD33 as a potential key mediator. Finally, summary-based MR analyses of both pleiotropic genes and anti-inflammatory drug target genes highlighted AMT, CRAT, ERAP2, ERBB3, GNL3, IRF3, MST1R, RPS26, SH2B1, SULT1A1, SULT1A2, TMEM258, CYP2D6 and MAPK3 as promising therapeutic targets for both cognitive function and autoimmune disorders. This study delineates the shared genetic architecture underlying the cognition-immune nexus and identifies novel candidate targets, highlighting the value of integrative genetic approaches for advancing diagnosis and treatment. - Source: PubMed
Publication date: 2026/07/01
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