RBM35A Blocking Peptide
- Known as:
- RBM35A Blocking Peptide
- Catalog number:
- 33r-6542
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- RBM35A Blocking Peptide
Related genes to: RBM35A Blocking Peptide
- Gene:
- ESRP1 NIH gene
- Name:
- epithelial splicing regulatory protein 1
- Previous symbol:
- RBM35A
- Synonyms:
- FLJ20171
- Chromosome:
- 8q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-22
- Date modifiied:
- 2019-02-20
Related products to: RBM35A Blocking Peptide
Related articles to: RBM35A Blocking Peptide
- The corpus luteum number in sows is a key reproductive indicator for measuring ovulation rate and reproductive efficiency. Its formation is precisely regulated by a complex gene regulatory network composed of multi-level molecular interactions. To systematically elucidate the molecular basis of this trait, this study comprehensively analyzed genes located within QTL for corpus luteum number. This approach identified a series of key regulatory molecules specifically expressed in the ovary, including transcription factors (TFs), long non-coding RNAs (lncRNAs), and microRNAs (miRNAs). Using bioinformatics methods to predict the target genes of candidate miRNAs, combined with functional enrichment analysis, revealed that these target genes were significantly enriched in multiple core reproductive pathways closely related to cell proliferation, differentiation, and hormone regulation, including the ErbB signaling pathway, PI3K-Akt signaling pathway, and TGF-beta signaling pathway. Based on the above findings, this study ultimately constructed a TF-lncRNA-miRNA-mRNA network, which is associated with QTL for corpus luteum number. Furthermore, key genes were validated via quantitative real-time PCR (qRT-PCR). Significant positive correlations were identified between the transcription factor and lncRNA , along with its potential target gene , as well as between transcription factor and lncRNAs (, ) and their potential target genes (, ). In addition, the functional validation results showed that the interference of significantly reduced the proliferation ability of sGCs. These key genes represent potential targets for genetic improvement of sow reproduction. - Source: PubMed
Publication date: 2026/06/01
Wang MiaomiaoLu MinGao YajieWang ChenxuXu TengtengYang ChenLiu Yong - Somatotropinomas are a subtype of pituitary adenomas that have a particular predilection to invade the cavernous sinus. The objective of this systematic review was to examine the evidence regarding the molecular basis for cavernous sinus invasion in somatotropinomas. This review was conducted in accordance with the 2020 PRISMA guidelines on 13 April 2025. Inclusion criteria were reports of associations between somatotropinoma molecular changes and cavernous sinus invasion in adult patients. Title/abstract screening and full-text screening were performed, with studies assessed for risk of bias using the Newcastle-Ottawa scale. A total of 43 studies were identified, encompassing 1,824 patients (724 invasive tumours). Overall, 33 studies identified molecules that were upregulated in invasive tumours and 20 studies identified molecules that were downregulated. Few studies incorporated modern proteomic or transcriptomic techniques. Risk of bias was low with a mean Newcastle-Ottawa scale score of 7.0 (±0.6). Molecules associated with invasion were related to epithelial-mesenchymal transition (E-cadherin, ESRP1, fascin-1, and MMP-9), cellular proliferation (PTTG, AIP, TCERG1, EIF2β, E2F1, Notch 2, STAT3, ARRB1, TGFB1, SMAD3, SOX9, SGK1, MAGEA6 DLL3, EGFL7, and pEGFR), hormonal signalling (GNAS, DRD5, DRD1, sst5TMD4, SSTR2, and SSTR5), and tumour angiogenesis (VEGF and Drp1). These molecular variations present a possible explanation for the proclivity of somatotropinomas for the cavernous sinus. Identified molecules represent options for novel targeted therapies or biomarkers that could inform prognostication. Modern proteomic and transcriptomic techniques and larger somatotropinoma datasets are required to further elucidate the molecular pathways responsible for cavernous sinus invasion in somatotropinomas. - Source: PubMed
Publication date: 2026/05/11
Ovenden Christopher DillonCandy NicholasBacchi StephenSorvina AlexandraCastle-Kirszbaum MendelPoonnoose SantoshVrodos NikitasJukes AlistairSantoreneos StephenTorpy David JPsaltis AlkisDe Sousa Sunita - As the mechanosensitive sensory cells in the inner ear, hair cells are characterized by their apical, F-actin-filled stereocilia. The stereocilia are organized into a staircase-like pattern with rows of increasing height. The development and maintenance of stereocilia are tightly regulated, and deficits in this process usually lead to hearing loss. Recently, our group reported that RNA-binding proteins (RBPs), such as RBM24 and ESRP1, play essential roles in the inner ear hair cells. In the present work, we show that nucleolin (NCL), a highly conserved RBP, is required for stereocilia maintenance in inner ear hair cells. Ncl knockout leads to progressive stereocilia degeneration in the outer hair cells in a basal-to-apical gradient. Meanwhile, Ncl knockout results in progressive stereocilia fusion in the inner hair cells in an apical-to-basal gradient. As a result, these stereocilia deficits lead to hair cell loss and eventually cause hearing loss in Ncl conditional knockout mice. RNA-sequencing analysis identified several genes for which the mRNA level is affected by Ncl knockout. Among them are Espnl and Ptprq, which have been shown to play essential roles in stereocilia development and/or maintenance. Further investigations confirmed that NCL could directly bind to Espnl and Ptprq mRNAs, and that NCL could increase the stability of Espnl and Ptprq mRNAs. Together, our data demonstrate that NCL plays essential roles in stereocilia maintenance by regulating the stability of its target mRNAs. - Source: PubMed
Publication date: 2026/04/16
Zong WenYan KejiXing HaiyueZhang HaoqingZhang WenGao RuiPeng XiaonaLi TangliangWang ZhaoqiXu Zhigang - Circular RNAs are implicated in the pathogenesis of prostate cancer (PCa). However, their functions, biogenesis and molecular mechanisms remain largely elusive. Here we aimed to investigate the role of circPHGDH in PCa. Cellular behaviors were assessed by the colony formation assay, Transwell analysis, western blotting and Seahorse assay. The underlying mechanisms were investigated using a luciferase reporter assay, RNA pull-down and real-time quantitative PCR. The lactylation of ESRP1 was examined by RNA immunoprecipitation, immunoprecipitation and western blotting. Our results revealed that circPHGDH expression was upregulated in PCa tissues and cells. Furthermore, the knockdown of circPHGDH inhibited PCa cell proliferation, migration, invasion, epithelial-mesenchymal transition and glycolysis. Mechanistically, circPHGDH functioned as a sponge for miR-149, which in turn directly targeted RAP1B. The biogenesis of circPHGDH was regulated by the splicing factor ESRP1. The glycolytic product lactate stabilized ESRP1 by promoting its lactylation at the K43 site; conversely, circPHGDH knockdown suppressed ESRP1 lactylation. Moreover, the silencing of circPHGDH inhibited tumor growth and metastasis in vivo via the miR-149/RAP1B axis, whereas circPHGDH facilitated tumor progression. In conclusion, the lactylation-modified ESRP1/circPHGDH/miR-149/RAP1B axis drives the progression of PCa. These findings provide novel insights into the pathogenesis of PCa and suggest promising therapeutic targets for its treatment. - Source: PubMed
Publication date: 2026/02/27
Wang XiangYu LimeiQian XiaolingYu Zhenfei - Epithelial-mesenchymal plasticity encompasses a spectrum of epithelial and mesenchymal identity states that enable cells to adapt to changing biological contexts. While CD44 isoform usage and epithelial splicing regulators ESRP1/2 are well-characterized in cancer-associated epithelial-mesenchymal transition (EMT), their regulation across physiological, non-transformed identity states remains less well defined. Here, we employed a non-malignant human cellular system comprising primary dermal fibroblasts, induced pluripotent stem (iPS) cells, and iPS-derived mesenchymal stem cells (iPS-MSCs) to define discrete epithelial, intermediate epithelial/mesenchymal, and mesenchymal identity states positioned along an epithelial-mesenchymal identity axis. Morphological assessment, lineage marker profiling, and RT-qPCR analyses revealed reproducible population-level stratification of these states. CD44 expression and alternative splicing followed this hierarchy, with CD44s predominating in fibroblasts, broad variant exon inclusion in iPS cells, and intermediate patterns in iPS-MSCs. ESRP1 expression mirrored CD44 splicing architecture, and ESRP1 silencing in iPS cells induced a shift toward CD44s, confirming its functional contribution to epithelial-associated CD44 splicing. In contrast, Notch-related transcriptional readouts displayed distinct, context-dependent profiles across the examined identity states. Together, this study establishes a tractable non-transformed human model that captures selected molecular features associated with epithelial-mesenchymal plasticity beyond malignant contexts. - Source: PubMed
Publication date: 2026/01/24
Bajdak-Rusinek KarolinaDiak NataliaTrybus AnnaFus-Kujawa AgnieszkaSalamon MarcelinaOlszewski JanWójtowicz WeronikaRozwadowska-Kunecka Patrycja