MYBL2 & E2F1 Protein Protein Interaction Antibody Pair
- Known as:
- MYBL2 & E2F1 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0186
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MYBL2 & E2F1 Protein Interaction Antibody Pair
Related genes to: MYBL2 & E2F1 Protein Protein Interaction Antibody Pair
- Gene:
- E2F1 NIH gene
- Name:
- E2F transcription factor 1
- Previous symbol:
- RBBP3
- Synonyms:
- RBP3
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-29
- Date modifiied:
- 2016-10-05
- Gene:
- MYBL2 NIH gene
- Name:
- MYB proto-oncogene like 2
- Previous symbol:
- -
- Synonyms:
- BMYB, B-MYB
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2016-10-05
Related products to: MYBL2 & E2F1 Protein Protein Interaction Antibody Pair
Related articles to: MYBL2 & E2F1 Protein Protein Interaction Antibody Pair
- Alternative splicing (AS) and alternative polyadenylation (APA), as post-transcriptional regulatory mechanisms, are involved in various biological processes through the generation of transcript variants. However, genome-wide studies of AS and APA during spleen development are scarce. This study aimed to characterize transcript diversity and changes in transcript isoforms in the spleen at two developmental stages using full-length isoform sequencing integrated with short-read RNA sequencing. We revealed widespread transcript diversity and identified 17,294 unannotated transcripts, most of which originated from known genes in the current pig genome annotation. The top 500 genes with the highest isoform diversity were mainly associated with disease occurrence and immune function, as revealed by Kyoto Encyclopedia of Genes and Genomes enrichment analysis. We also observed changes in major transcript usage and polyadenylation site selection during spleen development. Our results indicated that genes regulated immunological development mainly by switching dominant transcript isoforms rather than altering overall expression levels. In addition, genes exhibited a tendency of age-dependent preference for distal polyadenylation sites. Furthermore, transcription factors important for spleen development were identified, and the regulatory axes MYBL2/WEE1 and E2F1/WEE1 were constructed for the first time using molecular biology techniques. These findings not only refined the current pig genome annotation, but also provided a foundation for exploring the molecular mechanisms responsible for spleen development. - Source: PubMed
Publication date: 2026/03/10
Cui JinghaoZhu RongruSong MengkeSun YuanluPang YuTian MingHe XinmiaoLiu DiYang Xiuqin - Cervical cancer is the leading malignancy among women worldwide, posing clinical and public health challenges. This study aims to identify potential diagnostic biomarkers, therapeutic targets, and prognostic markers associated with cervical cancer through integrative bioinformatics approaches. - Source: PubMed
Publication date: 2025/12/01
Nezamabadi Farahani LeilaKazemnejad AnoshirvanAfrasiabi MahlaghaTapak Leili - (1) Background: Hepatocellular carcinoma (HCC) remains a major cause of cancer mortality and is characterized by pronounced inter- and intra-tumoral heterogeneity and therapy resistance. We aimed to define core transcriptional circuits that drive HCC malignancy and to delineate how these programs shape the tumor microenvironment (TME). (2) Methods: We integrated single-cell, spatial, and bulk transcriptomic datasets from public cohorts. (3) Results: We identified nine tumor-restricted transcription factors (TFs)-HTATIP2, HES6, ILF2, E2F1, MYBL2, DDIT3, FOXM1, HMGA1, and ETV4-whose expression and regulon activity associated with malignant phenotypes and poor survival. These TFs organize a progression axis from an early proliferative state (cluster C4) toward an invasive, metabolically adapted state (cluster C1) enriched for hypoxia, epithelial-mesenchymal transition (EMT), and inflammatory signaling. The C1 state remodeled the TME by establishing an immunosuppressive niche marked by expansion of T regulatory cells (Treg) and by accumulation of SPP1 macrophages. These macrophages, recruited and polarized by C1 tumor cells, exhibited M2-like, pro-angiogenic, and immunosuppressive features and engaged epithelial, immune, and stromal partners via SPP1-CD44 and SPP1-integrin interactions. (4) Conclusions: In summary, a tumor-intrinsic TF network cooperates with SPP1 macrophage signaling to promote a permissive microenvironment and HCC progression. This integrated axis highlights tractable vulnerabilities for therapeutic intervention. - Source: PubMed
Publication date: 2025/11/26
Lee Sang HoonAhn Ju WonChoi WonbinKim JinaHwang Joon YeonKim Jae-HwanKim HyaekangKwak Woori - Cellular senescence is intimately tied to tumorigenesis and progression, yet its exploration in meningiomas remains inadequate. In this study, we aim to unravel the role of cellular senescence-associated genes (CSA-genes) in meningioma recurrence and identify potential diagnostic markers and therapeutic targets. - Source: PubMed
Publication date: 2025/09/29
Huang Jian-HuangChen YaoKang Yuan-BaoLin Cai-Hou - Hormone-sensitive cancers (HSCs) are one of the predominant types of cancer leading to death globally. The current study has attempted to discover a potential therapeutic target that could be used against HSCs in women, namely, breast, ovarian, and endometrial cancer. The differentially expressed genes in each cancer type were compared with previously reported tamoxifen resistance-causing genes. The hub genes CCNA2, CDCA8, ISG15, and E2F1 were found in breast cancer, CCNA2, CDCA8, CXCR4, and LYN were found in ovarian cancer, and CCNA2 and POLE2 were found in endometrial cancer. The clusters with the hub genes were screened for functional importance and were found to be significant in cell cycle regulation pathways. The expression significance, correlation, mutational profile, survival potency, treatment response status, and clinical profile revealed that CCNA2 was significantly associated with all three cancers. This study revealed that CCNA2 was positively correlated with other resistance-causing genes such as CENPE, MK167, CDCA8, NEK2, PRC1, ZWINT, CDKN3, MYBL2, and E2F1, in various cancers, validating its potential to cause resistance. Compared with other hub genes, CCNA2 had a Lower mutation percentage and critical hazard ratios of 2.16, 1.75, and 1.68 in breast, ovarian, and endometrial cancers, respectively, indicating its pivotal role in survival. The median CCNA2 expression level was 21.301 in stage IV BC patients, 38.481 in stage II ovarian cancer patients, and 23.206 in stage IV endometrial cancer patients. Thus, CCNA2 could be a potential therapeutic target for treating HSCs with endocrine therapy resistance. - Source: PubMed
Publication date: 2025/09/11
Anbarasu SuvithaAnbarasu Anand