Human ErbB2 _ CD340 Protein Vector: HEK293
- Known as:
- Human ErbB2 _ CD340 Protein Vector: HEK293
- Catalog number:
- 10064-H01H
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human ErbB2 _ CD340 Protein Vector: HEK293
Related genes to: Human ErbB2 _ CD340 Protein Vector: HEK293
- Gene:
- ERBB2 NIH gene
- Name:
- erb-b2 receptor tyrosine kinase 2
- Previous symbol:
- NGL
- Synonyms:
- NEU, HER-2, CD340, HER2
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: Human ErbB2 _ CD340 Protein Vector: HEK293
Related articles to: Human ErbB2 _ CD340 Protein Vector: HEK293
- Overexpression and abnormal activation of membrane proteins promote malignant tumor cell proliferation, while traditional interventions are often limited by drug resistance caused by target mutations. Here, we designed a stimulus-responsive DNA tetrahedron lysosome-targeted chimera (tFNA-LYTAC) strategy for degrading embrane proteins. Two tetrahedra are modified with trivalent HER2 aptamers (tFNA1-Apt) and trivalent IGF2R aptamers (tFNA2-Apt), enabling targeted binding to HER2 and IGF2R, and are then self-assembled into tFNA-LYTAC under VEGF stimulation to promote HER2 degradation. The trivalent aptamer modification strategy significantly enhances the overall binding capacity of tFNA1-Apt to cells. Importantly, tFNA-LYTAC formed only in the presence of VEGF, integrating tetrahedral multivalent aptamer targeting with stimulus responsiveness to improve the degradation specificity. VEGF-responsive tFNA-LYTAC promoted HER2 degradation and suppressed the phosphorylation of key downstream signaling proteins. The study innovatively proposes a "target recognition-stimulus response-endocytic degradation" mode that selectively regulates membrane proteins through programmable multivalent aptamer nanostructures. - Source: PubMed
Song LuluZhou MiaomiaoWang YaGuo XiaoliYang XinyiHu YiqiongWang YifuYu SongchengLiu WeiHe Leiliang - Human epidermal growth factor receptor 2 (HER2) has emerged as a potential therapeutic target in bladder cancer (BC), particularly with the advent of next-generation antibody-drug conjugates (ADCs) like trastuzumab deruxtecan (T-DXd). However, the complex relationship between HER2 protein expression, genetic status, and clinical outcomes remains incompletely understood. We conducted an integrated multi-omics analysis of 445 BC cases (306 muscle-invasive [MIBC] and 139 non-muscle-invasive [NMIBC]) from the OMPU-NCC cohort, a uniform Japanese clinical database. The study utilized whole-exome sequencing, RNA sequencing, and refined HER2 immunohistochemistry (IHC) scoring. HER2 IHC positivity (1+/2+/3+) was identified in 30.1% of the cohort. An additional 8.5% exhibited faint membrane staining despite being IHC 0, indicating that detectable HER2 membrane staining was present in approximately 38.5% of cases. HER2 IHC scores showed no prognostic value, whereas ERBB2 amplification, detected in 7.8% of cases, was associated with poorer survival and remained an independent adverse prognostic factor in multivariable analysis (HR, 1.76; 95% CI: 1.08-2.87). ERBB2 amplification was accompanied by frequent co-amplification of genes within the 17q12 amplicon, including GRB7, MIEN1, and PGAP3. Molecular subtyping revealed that ERBB2 amplification was enriched in the Luminal Unstable (LumU) subtype. In contrast, detectable HER2 membrane staining significantly correlated with high NECTIN4 expression, indicating an overlap between tumors expressing these two ADC targets. HER2 protein expression and ERBB2 amplification represent distinct features of BC. Their integrated assessment may improve molecular stratification and guide future biomarker-driven studies. - Source: PubMed
Publication date: 2026/09/13
Hirosuna KensukeNishimura KazukiSakamoto MoritoshiTokushige SatoshiNakamori KeitaMatsunaga TomohisaYoshikawa YukiTsutsumi TakeshiMaenosono RyoichiTsujino TakuyaAjiro MasahikoAzuma HaruhitoYoshimi AkihideKomura Kazumasa - To provide a clinically oriented review of trastuzumab deruxtecan (T-DXd) in HER2-positive advanced gastric or gastroesophageal junction adenocarcinoma, focusing on evidence, post-progression HER2 reassessment, second-line sequencing, patient selection, regional implementation, and toxicity management. - Source: PubMed
Publication date: 2026/09/10
Sagawa TamotsuHirakawa MasahiroNagashima HiroyukiFujikawa Koshi - The pathogenesis of cancer is characterized by the acceleration of tumor growth, inhibition of tumor suppression, genetic and epigenetic alteration, lubricative transformation and tumor microenvironment. Extramammary Paget's disease (EMPD) is a rare skin cancer that originates from apocrine glands in genital and axillary area. Although the pathogenesis of EMPD is still poorly understood, increasing evidence reveals that the mechanism of EMPD progression is regulated by the acquired ability of EMPD cells and tumor microenvironment. HER2/PI3K/AKT signaling and hormone receptor pathways are activated. Whereas tumor mutation burden is low, numerous driver genes such as ERBB2 and PIK3CA are detected. Tumor evolution in EMPD is characterized by high genetic intratumor heterogeneity with shared background factors. Tumor microenvironment in EMPD promotes immune evasion through the reduction of reduced CD4 + and CD8 + T cells and the increase of Treg cells and CD163 + macrophages. Enhanced Warburg effect and S. aureus contribute to the suppression of antitumor immunity. This review focuses on the mechanism of malignant progression in EMPD (hallmarks of EMPD). - Source: PubMed
Publication date: 2026/09/10
Kajihara Ikko - Human epidermal growth factor receptor 2 (HER2)-positive breast cancer exhibits high metastatic potential, linked not only to intrinsic cancer cell traits but also to critical crosstalk with the tumor microenvironment. However, the coevolutionary mechanisms between cancer cells and multiple stromal subpopulations in driving distant metastasis remain poorly understood. Therefore, this study aimed to explore the microenvironmental regulatory mechanisms of breast tumor-initiating cells and their roles in HER2-positive breast cancer metastasis. Integrated multi-omics analyses (spatial transcriptomics, metabolomics, spatial in situ analysis, and proteomics) were used to identify novel cell subpopulations and their interactions. High-throughput sequencing of exosomal microRNAs (miRNAs) and single-nucleus RNA from the same tissue was performed to explore the molecular mechanisms underlying cell crosstalk. In vitro experiments were conducted to verify the interaction between stromal cells and prominin 1 (PROM1) SMAD family member 5 (SMAD5) cells. In vivo murine breast cancer models were established to confirm the role of stromal subpopulations in pulmonary metastasis, and parabiosis assays were carried out to compare key cell subpopulations between tumor-bearing mice and normal mice. Clinical samples were analyzed to correlate key cell subpopulations with clinicopathological features and prognosis. A breast tumor-initiating subpopulation, PROM1 SMAD5 cells, and its interactions with stromal cells, specifically adiponectin (ADIPOQ) notch receptor 4 (NOTCH4) adipocytes and decorin (DCN) transmembrane 4 L six family member 1 (TM4SF1) fibroblasts, were identified by integrated multi-omics analyses. Mechanistically, these 2 stromal subpopulations delivered functional miRNAs and mediated coatomer protein complex subunit alpha (COPA)-dependent epidermal growth factor receptor (EGFR) activation in PROM1SMAD5 cells, thereby triggering the EGFR-SMAD5-cytochrome P450 family 3 subfamily A member 4 (CYP3A4) axis to induce partial epithelial-mesenchymal transition (pEMT) and metastasis. Additionally, stroma-secreted exosomal miR-671-3p down-regulated Claudin1 in PROM1SMAD5 cells, promoting their evolution into PROM1SMAD5Claudin1 subpopulations with enhanced stemness and metastatic potential. In vivo experiments confirmed that the 2 stromal subpopulations markedly promoted pulmonary metastasis, and the 3 identified subpopulations preferentially accumulated in the primary tumors, lymph nodes, and pulmonary metastatic lesions of tumor-bearing mice. Clinically, these 3 subpopulations form a "trinity niche", whose aggregation associated with HER2 positivity, high malignancy, and lymph node/pulmonary metastasis, and predicted poor prognosis. This study clarified the microenvironmental regulation of breast tumor-initiating cells and provided new insights into precision therapy. - Source: PubMed
Publication date: 2026/09/09
Yin HuijingWang WeiGe JingFan GuangjianShi JichaoTian YeKong DepingZhang FanyiWei JingZhan HongruiXu ZhenyuGe JintongWang ShuweiZhang ZhimingZheng YunnaZhu ZhifaZi QingzhenYao XiaohuaDing YantingSong BoLi RuizhiFan LimingYin HaoJiang YinghaoZhang ShaoqianFu XingningWang JingZhou YanXue HaihuaQiu YannanGe LingYang YuqinJin YinhuiLou BinbinDing ShuningZhang TaoWei DenghuiZhu Li