RBM9 Blocking Peptide
- Known as:
- RBM9 Blocking Peptide
- Catalog number:
- 33r-8884
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- RBM9 Blocking Peptide
Related genes to: RBM9 Blocking Peptide
- Gene:
- RBFOX2 NIH gene
- Name:
- RNA binding fox-1 homolog 2
- Previous symbol:
- RBM9
- Synonyms:
- HNRBP2, FOX-2, HRNBP2
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-12
- Date modifiied:
- 2017-09-13
Related products to: RBM9 Blocking Peptide
Related articles to: RBM9 Blocking Peptide
- Uveal melanoma (UM) is a deadly ocular malignancy with well-described genetic alterations that predict disease outcome. However, our current understanding of the biological underpinnings of high-risk uveal melanoma progression remains relatively limited. Using RNA expression profiles from 250 patients with UM, we identified 12 novel biomarkers associated with high-risk UM, with protein expression level validation of the top two candidates: the transcriptional regulator RBFOX2 and matrix protein COL9A3. Moreover, we investigated the functional contribution of COL9A3 via its overexpression in EIF1AX and BAP1 UM cell lines. Our data suggest that COL9A3 enhances cell motility and cell proliferation and alters morphology specifically in BAP1 UM cells. Furthermore, zebrafish xenograft studies revealed increased cell dissemination in a EIF1AX UM cell line upon overexpression of COL9A3, whereas a BAP1 UM cell line remained unchanged under wild-type conditions. Interestingly, RNA sequencing revealed a high-stress profile by upregulated metabolic activity and loss of protein translation due to COL9A3 overexpression. BAP1 UM appears to adapt to this stress by upregulation of plasticity markers, such as CD44, Nestin, EZH2, ABCB5, PAX3 and CD166, as a coping mechanism. These markers are known as differentiation markers during the development of melanocyte biogenesis and are implicated in plasticity in other high-risk cancers. The relationship between COL9A3 and plasticity was validated by multiplex immunohistochemistry of formalin-fixed paraffin-embedded (FFPE) tissue, which demonstrated colocalization of COL9A3, CD44 and Nestin. BAP1-UM samples presented higher levels of COL9A3, CD44 and Nestin expression than EIF1AX or SF3B1 UM samples based on the mean fluorescent intensity of each marker. A positive correlation between COL9A3 and Nestin expression in triple-positive cells, irrespective of the UM subtype, was observed. Collectively, our findings suggest that COL9A3 is a novel high-risk biomarker that may contribute to UM cell plasticity and is most prevalent in BAP1 UM. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/07/21
van den Bosch QccVerdijk R MFadlelseed Hvan den Bosch TppOwens SKennedy SKilic EBrosens E - Neutrophil extracellular traps (NETs) are increasingly recognized as key regulators of tumor progression, yet the molecular circuitry that governs their induction in cancer remains elusive. Here, we identify the RNA-binding protein RBFOX2 as a tumor suppressor that curtails glioma growth by coordinately restraining tumor cell proliferation and NETosis. RBFOX2 expression is markedly reduced in glioma and positively correlates with patient survival. Mechanistically, RBFOX2 binds to 5-hydroxymethylcytidine (5hmC)-modified sites within PDGFB mRNA and promotes its decay, thereby dampening AKT-SP1 signaling and repressing CSF3 transcription. This repression limits neutrophil-mediated NET formation in the tumor microenvironment, as confirmed in PAD4 mice and upon CSF3 neutralization. Collectively, our study uncovers a 5hmC-dependent post-transcriptional mechanism linking RBFOX2 to NETosis control and glioma suppression, revealing RBFOX2 as a potential biomarker and therapeutic lever and establishing a broader paradigm in which RNA-binding proteins couple post-transcriptional RNA modification and immune regulation in tumor evolution. - Source: PubMed
Publication date: 2026/06/11
Chen XiDai WeiweiWang HanlinFang JianingYin BowenLiu ChangweiChen YulingWu RuixinCai YihengBian ShashaHai RihanLi JinZhu YiqianShu Minfeng - Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide. Aberrant expression of RNA binding fox-1 homolog 2 (RBFOX2) has been implicated in tumorigenesis and progression; however, its biological functions and clinical significance in CRC remain poorly understood. This study aimed to elucidate the role of RBFOX2 in CRC. - Source: PubMed
Publication date: 2026/05/31
Liu WenDongDai GuangMingLiao GuoLongOuyang PengHuang JinTuanXu Meng - Treatment-induced neuroendocrine prostate cancer (NEPC) represents an aggressive form of castration-resistant prostate cancer (CRPC) associated with lineage plasticity and therapeutic resistance. In this study, we investigated the role of the Hippo signaling axis in the transdifferentiation from androgen receptor-positive prostate cancer (ARPC) to NEPC. RNA sequencing analyses of CRPC metastases revealed coordinated alterations in Hippo pathway components, with decreased expression of YAP1, LATS2, and TEAD2 and increased expression of LATS1, TEAD1, and the RNA splicing regulator RBFOX2 in NEPC. These transcriptional alterations were consistently observed across multiple model systems and patient samples. Epigenetic analyses demonstrated that reduced expression of YAP1, TEAD2, and LATS2 was associated with increased DNA methylation, whereas elevated TEAD1 expression correlated with DNA hypomethylation in NEPC. NEPC selectively retained TEAD1 expression, including a spliced isoform not detected in ARPC. Proteomic interactome analyses revealed that TEAD1 associated with RNA splicing factors and DNA repair proteins. Functional studies showed that TEAD1 knockdown led to the reversion of gene programs associated with epithelial differentiation. These findings indicate that the conversion of ARPC to NEPC involves coordinated loss of AR, YAP1, and REST activity alongside sustained TEAD1 expression and altered RNA processing. Our data identify TEAD1 as a transcriptional regulator associated with the NEPC state and suggest a role for TEAD1-linked transcriptional and post-transcriptional mechanisms in prostate cancer lineage plasticity. - Source: PubMed
Publication date: 2026/05/30
Brown Lisha GColeman Ilsa MChu Tony L HSayar ErolcanPatel Radhika AHanratty BrianAdil MohamedLi DapeiLi YongtaoNguyen Holly MSessions Conner JSweeney Erin LAlumkal Joshi Jda Costa Rui M GilWang YuzhuoLin Daniel WTrue Lawrence DDumpit RuthCorey EvaLee John KNelson Peter SXin LiHaffner Michael CMorrissey Colm - The RhoBTB1/Cullin-3 (CUL3) pathway in smooth muscle cells (SMCs) controls the ubiquitination and proteasomal degradation of target proteins that regulate vasodilation, vasoconstriction, and the actin cytoskeleton and, through this, blood pressure (BP) and arterial stiffness. Using proximity labeling coupled with mass spectrometry in A7R5 SMCs, we identified proteins that bound to the C-terminal half of RhoBTB1, which functions as an adaptor to deliver substrates to CUL3. We examined the physiological relevance of one of these substrates, RbFox2. Coimmunoprecipitation validated the interaction of RbFox2 with RhoBTB1. RbFox2 expression was elevated in response to inhibition of the ubiquitination-proteasomal pathway, CUL3 deficiency, and RhoBTB1 inhibition by either siRNA or angiotensin II (ANG). RbFox2 was ubiquitinated in a RhoBTB1- and CUL3-dependent manner, suggesting its regulation through the RhoBTB1/CUL3-dependent ubiquitin-proteasome pathway. Inhibition of RbFox2 impaired the actin cytoskeleton in A7R5 cells and in primary SMCs from RbFox2fl/fl mice and decreased the levels of globular and filamentous actin. ANG increased BP and arterial stiffness of RbFox2fl/fl mice, but the progression of arterial stiffness was halted after SMC-specific RbFox2 deletion despite a continued rise in BP. We conclude that RhoBTB1 and RbFox2 are important regulators of arterial stiffness through a mechanism that influences cytoskeletal integrity. - Source: PubMed
Publication date: 2026/04/02
Kumar GauravChaihongsa NisitaBrozoski Daniel TGolosova DariaVazirabad IbrahimLu Ko-TingWackman Kelsey KSingh Ravi KSigmund Curt D