FGF3 Over-expression Lysate Product
- Known as:
- FGF3 Over-expression Lysate Product
- Catalog number:
- GWB-9FE056
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- FGF3 Over-expression Lysate Product
Related genes to: FGF3 Over-expression Lysate Product
- Gene:
- FGF3 NIH gene
- Name:
- fibroblast growth factor 3
- Previous symbol:
- INT2
- Synonyms:
- HBGF-3
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: FGF3 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: FGF3 Over-expression Lysate Product
- Vulvar squamous cell carcinoma (VSCC) comprises biologically distinct subtypes with divergent molecular profiles and clinical behaviors. In this study, we performed comprehensive genomic profiling of 48 primary VSCCs, integrating mutational and copy number data with HPV status and clinicopathological parameters. Tumors were stratified into HPV-associated (HPVA), HPV-independent (HPVI), and a third proposed subgroup characterized by HPV negativity and wild-type TP53 status. Overall, 650 somatic mutations were identified, with TP53, TERT promoter, NOTCH1, PIK3CA, and CDKN2A being the most frequently altered genes. HPVA VSCCs exhibited a higher mutational burden and enrichment of PIK3CA, NOTCH1, and MLL2 mutations, consistent with APOBEC-driven mutagenesis. HPVI VSCCs showed frequent TP53, TERTp, and CDKN2A mutations, along with an age-related mutational signature. Copy number alterations were more common in HPVI tumors, with recurrent amplifications in CCND1, FGF3/4/19, and CDK pathway genes. Six VSCCs lacked both HPV association and TP53 mutations, supporting the existence of a third molecular subtype, with frequent TERTp mutations and limited additional alterations. No significant survival differences were observed between subtypes, although nodal status remained prognostically relevant. These findings refine the molecular taxonomy of VSCC, support the recognition of a third genomic subgroup, and highlight subtype-specific therapeutic targets. - Source: PubMed
Publication date: 2026/05/11
Choschzick MHoesli LStergiou CRüschoff J H - Copy number variation (CNV), including genomic gains or losses of DNA segments ranging from kilobases to megabases, represents a major source of genetic diversity and can substantially alter gene dosage, regulation, and phenotype. Although CNVs have been catalogued across many dog breeds in prior large-scale efforts, breed-specific CNVs, defined as copy-number changes that are highly prevalent within one breed but rare or absent across others, have not been systematically investigated. To address this gap, we analyzed whole-genome sequencing data from 436 dogs representing 105 modern breeds and constructed a high-resolution catalog of breed-specific CNVs. - Source: PubMed
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Qin XiaoXu LinWang XiaozhenQi YouchaoZhong WeiShang BinWang ZhouChen Gang - Anaplastic lymphoma kinase () rearrangement has been identified in approximately 1% of lung squamous cell carcinomas (LUSCCs). Due to its rarity, the efficacy of anaplastic lymphoma kinase-tyrosine kinase inhibitors in the treatment of -positive LUSCCs is poorly characterized. - Source: PubMed
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