BRCA1 (Phospho-Ser1457) Antibody
- Known as:
- BRCA1 (Phospho-Ser1457) Antibody
- Catalog number:
- 11787
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- BRCA1 (Phospho-Ser1457) Antibody
Related genes to: BRCA1 (Phospho-Ser1457) Antibody
- Gene:
- BRCA1 NIH gene
- Name:
- BRCA1 DNA repair associated
- Previous symbol:
- -
- Synonyms:
- RNF53, BRCC1, PPP1R53, FANCS
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1991-02-20
- Date modifiied:
- 2019-04-23
- Gene:
- BRCA1P1 NIH gene
- Name:
- BRCA1 pseudogene 1
- Previous symbol:
- -
- Synonyms:
- LBRCA1, PsiBRCA1, pseudo-BRCA1
- Chromosome:
- 17q21
- Locus Type:
- pseudogene
- Date approved:
- 2005-05-26
- Date modifiied:
- 2005-08-09
Related products to: BRCA1 (Phospho-Ser1457) Antibody
Related articles to: BRCA1 (Phospho-Ser1457) Antibody
- Pseudogenes have been regarded as nonfunctional byproducts of evolutionary processes. However, emerging evidence indicates that pseudogenes perform diverse biological roles in human physiology and pathology. We identified the pseudogene (), a fusion pseudogene derived from the tumor suppressor and ribosomal protein genes, as an immunoregulatory RNA in breast cancer. In this study, we show that expression varies across multiple cancer cell types, with no significant association with or somatic mutations in breast and ovarian tumors. Interestingly, inhibition elicits antitumor effects in multiple cancer cell types and preclinical tumor models through an antiviral defense mechanism. Loss of induces antiviral gene expression, promotes apoptosis, and increases sensitivity to chemotherapy in various cancer cells, without inducing apoptosis in nonmalignant cells. This antiviral response also enhances macrophage-mediated phagocytosis of -deficient cancer cells. Mechanistically, the majority of transcripts are circular RNAs and regulate NF-κB-driven antiviral gene expression. Furthermore, intratumoral expression of is elevated in tumor cells, compared to normal breast tissue, and its depletion significantly inhibits the growth of both primary and metastatic breast tumor organoids. Finally, in a humanized mouse model of breast cancer, loss stimulates antiviral gene expression and increases T cell infiltration into tumors. These findings support a critical role for in regulating innate immune defense and antitumor responses across cancer types, suggesting that targeting pseudogene-derived RNAs may offer innovative therapeutic strategies to enhance antitumor immunity in breast and other cancers. - Source: PubMed
Publication date: 2026/05/04
Han Yoo JaneZhang JingShariff MaryamWu SulinKhramtsova GalinaNguyen Long ChiPeiffer Daniel SLi NanshengLewicka AnnaMoore MatthewPiccirilli Joseph AOlopade Olufunmilayo I - Innate immune defense mechanisms play a pivotal role in antitumor responses. Recent evidence suggests that antiviral innate immunity is regulated not only by exogenous non-self-RNA but also by host-derived pseudogene RNAs. A growing body of evidence also indicates a biological role for pseudogenes as gene expression regulators or immune modulators. Here, we report an important role for , the pseudogene of the tumor-suppressor gene, in regulating innate immune defense mechanisms in breast cancer cells. expresses a long-noncoding RNA (lncRNA) in breast cancer cells through divergent transcription. Expression of lncRNA- is increased in breast tumors compared with normal breast tissues. Depletion of induces an antiviral defense-like program, including the expression of antiviral genes in breast cancer cells. Furthermore, -deficient cancer cells mimic virus-infected cells by stimulating cytokines and inducing cell apoptosis. Accordingly, depletion of increases host innate immune responses and restricts virus replication. In converse, overexpression of reduces cytokine expression in breast cancer cells. Mechanistically, lncRNA- is localized in the nucleus, binds to the NF-κB subunit RelA, and negatively regulates antiviral gene expression. Finally, in a xenograft mouse model of breast cancer, depletion of stimulates cytokine expression and local immunity, and suppresses tumor growth. Our results suggest an important role for in innate immune defense mechanisms and antitumor responses. This mechanism of antiviral immunity regulated by a host-derived pseudogene RNA may guide the development of novel therapies targeting immune responses in breast cancer. SIGNIFICANCE: This study identifies a novel mechanism of innate immunity driven by a host pseudogene RNA that inhibits innate immune defense mechanisms and antitumor responses through regulation of antiviral gene expression. - Source: PubMed
Publication date: 2021/01/20
Han Yoo JaneZhang JingLee Jung-HyunMason Jennifer MKarginova OlgaYoshimatsu Toshio FHao QinyuHurley IanBrunet Laia ParéPrat AleixPrasanth Kannanganattu VGack Michaela UOlopade Olufunmilayo I - In recent years, the number of patients being offered BRCA1/2 testing has changed dramatically. Advances in high-throughput sequencing technology have led many diagnostic laboratories to test next-generation sequencing (NGS)-based platforms as the main technology for clinical testing. As a consequence, the proportion of novel BRCA1/2 variants detected has greatly increased. Here, we describe two novel BRCA1 large deletions detected in Italian patients affected by hereditary breast and ovarian cancer syndrome (HBOC). - Source: PubMed
Rizza RobertaHackmann KarlParis IdaMinucci AngeloDe Leo RossellaSchrock EvelinUrbani AndreaCapoluongo EttoreGelli GianfrancoConcolino Paola - The duplication in the primate lineage of a portion of the breast and ovarian cancer susceptibility gene BRCA1 has created a BRCA1 pseudogene 45 kb away. Non-allelic homologous recombination (NAHR) between BRCA1 and BRCA1P1 has generated recurrent deleterious germ-line 37-kb deletions encompassing the first two exons of BRCA1, accounting for several breast and ovarian cancer families in various populations. In principle, NAHR intermediates resolution could also lead through a non-crossover configuration to interlocus gene conversion (IGC), but none had been described as yet. Here, we report for the first time an IGC event identified in a breast and ovarian cancer family involving exactly the same segment as that involved in the 37-kb deletions. Close examination of the consequences of this IGC event showed that it does not impact BRCA1 expression. Detailed analysis of the regions of homology between BRCA1 and its pseudogene revealed the specificity of the segment where recombination systematically occurs. - Source: PubMed
Publication date: 2015/07/14
Tessereau ChloéLéoné MélanieBuisson MoniqueDuret LaurentSinilnikova Olga MMazoyer Sylvie