Ask about this productRelated genes to: RBM39 Blocking Peptide
- Gene:
- RBM39 NIH gene
- Name:
- RNA binding motif protein 39
- Previous symbol:
- RNPC2
- Synonyms:
- CC1.3, HCC1, CAPER, fSAP59, CAPERalpha
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-21
- Date modifiied:
- 2014-11-19
Related products to: RBM39 Blocking Peptide
Related articles to: RBM39 Blocking Peptide
- Despite the expression of multiple transcript isoforms from a gene, conventional gene expression analyses assume that a single transcript is expressed from each gene. We analyzed the transcript isoforms expressed in gonadotropin-induced mouse mural and cumulus granulosa cells (mGCs and cGCs) isolated from antral follicles to elucidate the potential mechanism of differentiation. Considering that either a single transcript or multiple isoforms are expressed from genes, we identified differential expression of about 70% of transcripts between mGCs and cGCs. Although the differential expressions were similar, the single-transcript-wise differentially expressed genes did not correlate with their corresponding differentially expressed transcript isoforms. We identified transcript isoforms of key transcriptional regulators in ovaries, including Chd1, Ezh2, Kdm5a/5b, Gata4, Esr2, Fos, Myc, and Ybx1, that were not identified in single-transcript-based analyses. Further analysis revealed a transcript switch in more than 30% of the differentially expressed isoforms. While one or more transcript isoforms of Cebpa, Dnmt3a, Pgr, Rest, Runx1, and Sirt1 were switched off, those of Brd7, Chd1, Med21, Nfkbia, Rbm39, Suv39h2, Tcf12, Xist, and Ybx3 were switched on in cGCs. Interestingly, several genes, including Dab2, Ezh2, Gata4, Gnas, Gtf2i, Klf10, Setdb1, and Sp3, exhibited at least one isoform that was switched off and another that was switched on in cGCs. Transcript switching was primarily due to alternative splicing, followed by alternative transcription start sites and polyadenylation sites. We also identified differential expression of the potential regulators of such transcript switching in cGCs. Our results suggest that transcript switching may play an important role in mural and cumulus granulosa differentiation, a key insight that would remain unknown without mRNA isoform analysis. - Source: PubMed
Publication date: 2026/05/23
Shila SharminPei Grace JBahadursingh ElizabethPeramsetty NikiDahiya VineshMarsh Courtney AThiyagarajan RamkumarZhang MeijiaFields Patrick ERumi M A Karim - Pulmonary arterial hypertension (PAH) is a progressive vascular disease characterized by immune dysregulation and pulmonary vascular remodeling. This study aimed to identify immune-associated hub genes in PAH using an integrative bioinformatics framework and to validate key candidates in an experimental model. - Source: PubMed
Publication date: 2026/05/22
Yang XitongZhou BinYang YingDong YuFu JifenLiu HongWu Xinhua - In recent years, the concept of "modality" has attracted significant attention in drug discovery, encompassing diverse approaches such as small molecules, antibodies, nucleic acids, and cell-based therapies. Eisai has leveraged its long-standing expertise in small-molecule drug design to focus on proximity-inducing compound (PIC), which induces novel pharmacological effects by bringing two distinct proteins into close proximity. PIC form ternary complexes between a target protein and an effector protein, enabling mechanisms such as targeted degradation, post-translational modification, and modulation of protein-protein interactions. This strategy allows intervention in previously "undruggable" targets that lack suitable binding pockets for conventional inhibitors. Among PIC, targeted protein degraders such as proteolysis targeting chimera (PROTAC) and molecular glue degrader (MGD) have advanced rapidly into clinical development worldwide. Eisai's entry into this field was driven by the discovery of the unique mechanism of action of Indisulam and E7820, which function as MGD to degrade RBM39 via DCAF15 recruitment. Building on this foundation, Eisai is pursuing tumor-selective strategies, including the development of a CEACAM6-targeted degrader antibody conjugate (DAC) and PROTAC utilizing tumor-selective E3 ligases. These approaches aim to achieve both efficacy and safety by restricting degradation activity to cancer cells. PIC represent a transformative modality that expands the druggable proteome and offers new therapeutic options for intractable diseases. This article outlines Eisai's efforts in PIC-based drug discovery, with a focus on targeted protein degradation and future perspectives. - Source: PubMed
Kira Kazunobu - Depletion of the splicing factor RBM39 disrupts spliceosome function and induces widespread RNA splicing defects, leading to antiproliferative effects in susceptible cancer cells. Here, we report the discovery and characterization of a new series of biphenyl-containing RBM39 degraders. The lead compound 42 promotes RBM39 degradation through formation of a ternary complex with RBM39 and DCAF15/DDB1 in a Cullin-RING E3 ligase- and proteasome-dependent manner, consistent with a molecular glue mechanism. Transcriptomic analyses in HCT-116 and K562 cells revealed extensive alternative splicing alterations and suppression of cell-cycle-associated pathways, resulting in G2/M-phase arrest without apoptosis. Comparative cellular profiling identified 41 (YSA64) as a potent analog in acute myeloid leukemia MV4-11 cells and Ewing sarcoma A673 cells, disease contexts that have been minimally explored for RBM39 degraders. Notably, 41 exhibited favorable oral pharmacokinetics and significant antitumor efficacy in MV4-11 xenograft models. Collectively, this work expands the chemical space of RBM39 degraders and supports their continued development as RNA splicing-targeted anticancer agents. - Source: PubMed
Publication date: 2026/05/02
Lyu XilinWang ZhiyiShen YanyanWang XianchengWang YixuanYu ShumengYang BiyuYan ZiqinZhang ShijieLu YuhangHuang HeChen YiZhao Yujun - Cigarette smoking significantly accelerates the initiation and progression of colorectal cancer (CRC), although the precise molecular mechanisms remain incompletely elucidated. Among tobacco-derived carcinogens, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a key one, which has been demonstrated to enhance the malignant progression of CRC. CUT&RUN-seq and mRNA-seq analyses, along with subsequent validation experiments, reveal that NNK upregulates the expression of the acetyltransferase p300. This, in turn, mediates an increase in H3K27ac modification levels at the ANKHD1 promoter, thereby promoting ANKHD1 expression. Furthermore, high expression of ANKHD1 is significantly correlated with poor prognosis in CRC patients. Phenotypic experiments demonstrate that, compared to p300 overexpression alone, combined p300 overexpression with ANKHD1 knockdown partially suppresses the proliferation and metastatic capacity of CRC cells. This suggests that NNK may promote malignant CRC progression by upregulating the p300-ANKHD1 signaling axis. Further mechanistic investigations indicate that the scaffold protein ANKHD1 directly interacts with RBM39 to facilitate the splicing and expression of MKI67 pre-mRNA, thereby driving the malignant progression of NNK-exposed CRC cells. In summary, this study provides novel insights, proposing that targeting the p300-mediated H3K27ac modification pathway to suppress ANKHD1 expression may represent a promising therapeutic strategy and prognostic marker for CRC patients with a history of smoking. - Source: PubMed
Publication date: 2026/04/28
Jiang MinZhao YutingMa QunDing KunHuang YefeiChen Yansu