Ask about this productRelated genes to: E2f7 Blocking Peptide
- Gene:
- E2F7 NIH gene
- Name:
- E2F transcription factor 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-11
- Date modifiied:
- 2018-11-15
Related products to: E2f7 Blocking Peptide
Related articles to: E2f7 Blocking Peptide
- Non-invasive assessment of oocyte quality remains a challenge in assisted reproductive technology (ART). Through their bidirectional communication with the gamete, cumulus cells (CCs) act as a functional mirror of oocyte competence; however, the specific angiogenic signature within this microenvironment is still poorly understood. In the present study, we performed RNA-seq on CCs from healthy oocyte donors and infertile patients, utilizing a multi-pipeline bioinformatic approach (STAR-Cufflinks, TopHat-HTSeq, and HISAT2-StringTie) to establish a high-confidence, exploratory transcriptomic profile. A set of 234 differentially expressed genes (DEGs) consistently identified across pipelines was obtained, with functional enrichment highlighting blood vessel morphogenesis and angiogenesis as primary drivers of transcriptomic divergence between groups. RT-qPCR validation in individual samples confirmed statistically significant differences for (upregulated) and (downregulated) in infertile patients, while other angiogenesis-related genes, including , and , showed consistent but non-significant expression trends, suggesting alterations in angiogenesis-related processes within the follicular microenvironment. These findings support the presence of coordinated angiogenesis-related alterations in cumulus cells and provide a basis for future studies exploring their potential relevance in oocyte competence and ART outcomes. - Source: PubMed
Publication date: 2026/04/11
Baratas AlejandroPérez-Quiroga VictoriaPlanello RosarioAquilino MónicaSerrano MagdalenaCasa Moisés de laFranco-Iriarte YosuRoy Rosa - Aberrant nucleocytoplasmic transport mediated by Exportin 1 (XPO1) contributes to leukemogenesis, yet the molecular basis underlying the limited efficacy of the XPO1 inhibitor Selinexor in acute myeloid leukemia (AML) remains unclear. This study aimed to define the role of XPO1 in AML and elucidate the mechanism by which Selinexor regulates homologous recombination (HR). - Source: PubMed
Publication date: 2026/04/23
Xu ChunliWang DandanChen RuiqiFeng XuCheng FengChen Yu - Chromatin remodeling proteins and transcription factors (TFs) play critical roles in the tumor biology of small cell lung cancer (SCLC). Genome-wide characterization of histone post-translational modifications (PTMs) and TF binding sites is essential for identifying regulatory DNA elements and gene pathways that will lead to a deeper mechanistic understanding of SCLC and nominate targets for therapeutic intervention. Cleavage Under Targets and Release Using Nuclease followed by next generation sequencing (CUT&RUN-seq) is a powerful method for mapping specific histone modifications and determining the DNA-binding profiles of a wide range of proteins in situ in the cellular genome. In CUT&RUN, the micrococcal nuclease (MNase) fused to Protein A/G is recruited via antibodies to the genomic locations of chromatin-associated proteins, where the underlying DNA fragments are released from bulk chromatin upon MNase activation and cleavage. This localized digestion generates small, locus-specific DNA fragments suitable for sequencing. Here, we present a detailed protocol for profiling histone modifications H3K4me3 (associated with active or open promoters) and H3K4me1 (associated with active enhancers), as well as the transcription factor E2F7, in SCLC. This protocol has been optimized for neuroendocrine (NE) SCLC cell line models, which are typically characterized by large nuclei, scant cytoplasm, and growth as non-adherent aggregates in suspension. - Source: PubMed
Publication date: 2026/04/03
Du MeijunAndrae Jaime WendtTschannen MichaelMathison AngelaJin VictorChen Hui-Zi - - Source: PubMed
Publication date: 2026/04/19
Gao XiangtingZhao ChengyiWang ShuyiLi Jinxia - - Source: PubMed
Publication date: 2026/04/17
Franklin OskarTorres Madeline B