GTF2F1 antibody - N-terminal region (P100810_P050)
- Known as:
- GTF2F1 (anti-) - N-terminal region (P100810_P050)
- Catalog number:
- p100810_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GTF2F1 antibody - N-terminal region (P100810_P050)
Related genes to: GTF2F1 antibody - N-terminal region (P100810_P050)
- Gene:
- GTF2F1 NIH gene
- Name:
- general transcription factor IIF subunit 1
- Previous symbol:
- -
- Synonyms:
- TFIIF, BTF4, RAP74, TF2F1
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-04
- Date modifiied:
- 2015-11-09
Related products to: GTF2F1 antibody - N-terminal region (P100810_P050)
Related articles to: GTF2F1 antibody - N-terminal region (P100810_P050)
- In this study, we systematically investigated bladder cancer-related gene signatures using a toxicogenomics-informed framework, with particular attention to genes associated with lactylation-related pathways. Multi-omics data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) were integrated, and Weighted Gene Co-expression Network Analysis (WGCNA), a toxicology database, and lactylation-related gene sets were combined for intersection screening. Machine learning algorithms, including LASSO, SVM, and random forest, were then applied to identify key genes. Four prioritized BPA-lactylation-associated candidate genes-ENO1, WBP11, GTF2F1, and SPR-were ultimately identified and showed consistent associations with metabolic, immune, and transcription-related features. Multi-level validation, including immune infiltration analysis, single-cell transcriptome localization, proteomic validation, and molecular docking and kinetic simulation, supported the structural plausibility of BPA-protein interactions at the molecular level. This study proposes a toxicogenomics-informed, hypothesis-generating framework that prioritizes candidate genes and pathways potentially linking BPA-related signatures with lactylation-associated processes in bladder cancer. - Source: PubMed
Publication date: 2026/05/05
Wang HaoLiu HongquanSun FengzeWu Jitao - Nonmuscle invasive bladder cancer (NMIBC) represents a significant clinical challenge due to its high recurrence and progression rates. We aimed to characterize proteomic differences between matched pairs of tumor and control bladder tissues in NMIBC to identify potential biomarkers and underlying molecular mechanisms. : Data-independent analysis proteomics experiments were conducted in paired samples from 45 patients with NMIBC, comprising 45 tumor and 45 control tissues. Tumor and nontumor results were compared using a paired Student's test. Proteins detected in at least 50% of the samples were used. : A total of 188 differentially abundant detected proteins were identified, along with 11 proteins exclusively detected in tumor tissues, including SPINT1, TXNDC12, GTF2F1, COPZ1, RS25, PTK2, LSR, SNRNP40, NCOA5, SEC63, and CD2AP. The protein interaction network analysis among this set of proteins revealed AGR2, FLNA, TPM1, and CALD1. Additionally, CNDP2 and CTSD expression were inversely correlated with tumor recurrence and progression risk respectively, while EPS8L2 and KRT7 levels were associated with tumor staging. : Our study identified specific proteins as potential NMIBC biomarkers and drug targets. The identified proteins, particularly those linked to tumor recurrence and staging, warrant further validation to assess their clinical utility in NMIBC diagnosis, prognosis, and treatment strategies. - Source: PubMed
Publication date: 2026/01/26
Silva Tiago AparecidoViana Luciana GodoyCarvalho Valdemir MelechcoBertolla Ricardo PimentaAntoniassi Mariana PereiraAzevedo Hatylas - Testicular differentiation of undifferentiated gonads is triggered by the SRY/Sry (sex-determining region of chromosome Y) gene on the Y chromosome in most mammals. SRY and NR5A1 (nuclear receptor subfamily 5, group A, member 1) proteins regulate transcription of the autosomal SOX9/Sox9 (SRY-box9) gene in XY embryonic gonads, inducing testicular differentiation. One exception, the Amami spiny rat (Tokudaia osimensis), lacks the Y chromosome and Sry. We previously reported that this species has a male-specific duplication upstream of Sox9, and an enhancer (tosEnh14) in the duplication regulates Sox9 transcription without Sry. However, tosEnh14 is not activated by NR5A1 alone, suggesting that another transcription factor(s) which binds to tosEnh14 is necessary. Because this species is endangered and heavily protected, it presents many challenges for genetic studies. Therefore, we explored novel transcription factors that regulate Sox9 via tosEnh14 using mouse samples. To detect proteins that bind to tosEnh14 DNA, Southwestern blotting analysis was performed using mouse embryonic gonad extracts. Bands of a similar molecular weight but prominent in males and faint in females were subjected to mass spectrometry analysis. Peptides derived from 174 genes were identified, and eight genes associated with gene ontology terms such as "DNA binding" and "regulation of transcription by RNA polymerase II" were selected. For further screening, the expression level of each gene was examined using single-cell RNA-sequencing data for mouse progenitor cells, which differentiate into Sertoli cells in mouse embryonic testes and granulosa cells in embryonic ovaries. Finally, five genes (Elf2, Etv6, Fiz1, Gtf2f1 and Trim27) encoding transcription factors, whose expression was confirmed in seminiferous tubules of E13.5 XY embryos by whole-mount in situ hybridization, were selected as candidates. Binding sites for ELF2 and ETV6 are present in the tosEnh14 DNA sequence. Our study contributes to understanding the molecular mechanisms underlying sex determination in mammals. - Source: PubMed
Publication date: 2025/06/05
Mitsukawa ShoichiroMizushima ShuseiKimura YukiKuroiwa Asato - Cisplatin-based chemotherapy is a cornerstone in treating cervical cancer, yet the efficacy is frequently limited by the rapid onset of drug resistance, a major challenge in clinical management. To investigate this, we employed HPV16+ human cervix squamous carcinoma cells, SiHa (CIS/S), and their cisplatin-resistant subline (CIS/R) as a model. Using DIA-based proteomics, we identified 5152 protein groups and over 50,000 peptides with a global FDR <1%. Comparative analysis revealed 123 differentially expressed proteins. Gene Set Enrichment Analysis (GSEA) highlighted proteins involved in DNA damage, metabolism, and repair pathways (RFC4, RFC3, RFC2, DUT, DDX54, CDCA8, CDK7, CHAF1B, and GTF2F1), suggesting a role in developing acquired cisplatin resistance. Pathways related to mitotic spindle assembly and P53 signaling were found to be perturbed in resistant cells. Next, we screened a library of approx. 240 FDA-approved drugs against three protein targets and found four small-molecular ligands as potential hits for further validation. Cabozantinib and sorafenib gave us positive results in terms of increasing the cisplatin sensitivity of CIS/R cells. In conclusion, our findings provide insights into the molecular mechanisms underpinning cisplatin resistance in cervical cancer and propose novel strategies for combating this resistance through targeted therapies and drug repurposing. - Source: PubMed
Publication date: 2025/04/29
Mukherjee AmritaManna SayanSingh AvinashRay AdrijaSrivastava Sanjeeva - The number of primordial follicles (PFs) in mammals determines the ovarian reserve, and impairment of primordial follicle formation (PFF) will cause premature ovarian insufficiency (POI). - Source: PubMed
Publication date: 2023/12/11
Tan Hang-JingDeng Zi-HengShen HuiDeng Hong-WenXiao Hong-Mei