Last update 19 Sep 2024

RNP

Last update 19 Sep 2024

Basic Info

Synonyms

FLJ20008, KIAA1839, RBM40

+ [10]

Introduction

Participates in pre-mRNA U12-dependent splicing, performed by the minor spliceosome which removes U12-type introns. U12-type introns comprises less than 1% of all non-coding sequences. Binds to the 3'-stem-loop of m(7)G-capped U12 snRNA.

Drugs associated with RNP

ATRC-101

Target

RNP

Mechanism

RNP inhibitors

Active Org.-

Originator Org.

Atreca, Inc.

Active Indication-

Inactive Indication

Acral Lentiginous Malignant Melanoma [+16]

Drug Highest PhaseSuspended

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with RNP

NCT04244552 / TerminatedPhase 1

A Phase 1b Dose Escalation and Expansion Trial to Investigate the Safety, Tolerability, Pharmacokinetics, and Biological Activity of ATRC-101 as Monotherapy and in Combination With Other Anticancer Agents in Adults With Advanced Solid Malignancies

ATRC-101-A01 is a Phase 1b, open-label dose escalation and expansion trial of ATRC-101, an engineered fully human immunoglobulin G, subclass 1 (IgG1) antibody derived from a naturally occurring human antibody. The safety, tolerability, PK, and biological activity of ATRC-101 will be characterized when administered every two weeks (Q2W) or every 3 weeks (Q3W) as a monotherapy or in combination with other anticancer agents.

Start Date11 Feb 2020

Sponsor / Collaborator

Atreca, Inc.

100 Clinical Results associated with RNP

100 Translational Medicine associated with RNP

0 Patents (Medical) associated with RNP

511

Literatures (Medical) associated with RNP

31 Dec 2024·Expert Review of Vaccines

Screening of tumor antigens and immunogenic cell death landscapes of prostate adenocarcinoma for exploration of mRNA vaccine

Article

Author: Gu, Xin ; Song, Shangqing ; Lu, Yingying ; Wang, Jianqing ; Zhan, Ming ; Xu, Bin ; Lin, Yuansheng ; Wang, Jiangyi ; Fei, Xiang ; Zhou, Lin ; Liu, Yushan ; Yang, Qing ; Yu, Guopeng ; Seo, Seung-Yong

BACKGROUNDIn this study, effective antigens of mRNA vaccine were excavated from the perspective of ICD, and ICD subtypes of PRAD were further distinguished to establish an ICD landscape, thereby determining suitable vaccine recipients.RESEARCH DESIGN AND METHODSTCGA and MSKCC databases were applied to acquire RNA-seq data and corresponding clinical data of 554 and 131 patients, respectively. GEPIA was employed to measure prognostic indices. Then, a comparison of genetic alterations was performed utilizing cBioPortal, and correlation of identified ICD antigens with immune infiltrating cells was analyzed employing TIMER. Moreover, ICD subtypes were identified by means of consensus cluster, and ICD landscape of PRAD was depicted utilizing graph learning-based dimensional reduction.RESULTSIn total, 4 PRAD antigens were identified in PRAD, including FUS, LMNB2, RNPC3, and ZNF700, which had association with adverse prognosis and infiltration of APCs. PRAD patients were classified as two ICD subtypes based on their differences in molecular, cellular, and clinical features. Furthermore, ICD modulators and immune checkpoints were also differentially expressed between two ICD subtype tumors. Finally, the ICD landscape of PRAD showed substantial heterogeneity among individual patients.CONCLUSIONSIn summary, the research may provide a theoretical foundation for developing mRNA vaccine against PRAD as well as determining appropriate vaccine recipients.

01 Oct 2024·Gene

Mapping cell diversity in human sporadic cerebral cavernous malformations

Article

Author: Yang, Yibing ; Qi, Tiewei ; Hou, Xiaocan ; Wang, Chuhuai ; Li, Jiaoxing ; Sheng, Wenli ; Liang, Feng

BACKGROUNDCerebral cavernous malformation (CCM) is a low-flow, bleeding-prone vascular disease that can cause cerebral hemorrhage, seizure and neurological deficits. Its inheritance mode includes sporadic or autosomal dominant inheritance with incomplete penetrance, namely sporadic CCM (SCCM) and familial CCM. SCCM is featured by single lesion and single affection in a family. Among CCM patients especially SCCM, the pathogenesis of the corresponding phenotypes and pathological features or candidate genes have not been fully elucidated yet.METHODSHere, we performed in-depth single-cell RNA sequencing (scRNA-Seq) and bulk assay for transposase-accessible chromatin sequencing (ATAC-Seq) in SCCM and control patients. Further validation was conducted for the gene of interest using qPCR and RNA in situ hybridization (RNA FISH) techniques to provide further atlas and evidence for SCCM generative process.RESULTSWe identified six cell types in the SCCM and control vessels and found that the expression of NEK1, RNPC3, FBRSL1, IQGAP2, MCUB, AP3B1, ESCO1, MYO9B and PVT1 were up-regulated in SCCM tissues. Among the six cell types, we found that compared with control conditions, PVT1 showed a rising peak which followed the pseudo-time axis in endothelial cell clusters of SCCM samples, while showed an increasing trend in smooth muscle cell clusters of SCCM samples. Further experiments indicated that, compared with the control vessels, PVT1 exhibited significantly elevated expression in SCCM samples.CONCLUSIONIn SCCM conditions, We found that in the process of development from control to lesion conditions, PVT1 showed a rising peak in endothelial cells and showed an increasing trend in smooth muscle cells at the same time. Overall, there was a significantly elevated expression of NEK1, RNPC3, FBRSL1, IQGAP2, MCUB, AP3B1, ESCO1, MYO9B and PVT1 in SCCM specimens compared to control samples.

01 Aug 2024·Advanced Science

Minor Spliceosomal 65K/RNPC3 Interacts with ANKRD11 and Mediates HDAC3‐Regulated Histone Deacetylation and Transcription

Article

Author: Zhou, Zhen-Zhen ; Jiang, Xi-Ping ; Li, Chen-Hui ; Li, Liang ; Fan, Yu-Jie ; Ding, Zhan ; Liang, Shao-Bo ; Wi, Kwang-Chon ; Huang, Qi-Wei ; Xu, Yong-Zhen ; Long, Ni

AbstractRNA splicing is crucial in the multilayer regulatory networks for gene expression, making functional interactions with DNA‐ and other RNA‐processing machineries in the nucleus. However, these established couplings are all major spliceosome‐related; whether the minor spliceosome is involved remains unclear. Here, through affinity purification using Drosophila lysates, an interaction is identified between the minor spliceosomal 65K/RNPC3 and ANKRD11, a cofactor of histone deacetylase 3 (HDAC3). Using a CRISPR/Cas9 system, Deletion strains are constructed and found that both Dm65KΔ/Δ and Dmankrd11Δ/Δ mutants have reduced histone deacetylation at Lys9 of histone H3 (H3K9) and Lys5 of histone H4 (H4K5) in their heads, exhibiting various neural‐related defects. The 65K‐ANKRD11 interaction is also conserved in human cells, and the HsANKRD11 middle‐uncharacterized domain mediates Hs65K association with HDAC3. Cleavage under targets and tagmentation (CUT&Tag) assays revealed that HsANKRD11 is a bridging factor, which facilitates the synergistic common chromatin‐binding of HDAC3 and Hs65K. Knockdown (KD) of HsANKRD11 simultaneously decreased their common binding, resulting in reduced deacetylation of nearby H3K9. Ultimately, this study demonstrates that expression changes of many genes caused by HsANKRD11‐KD are due to the decreased common chromatin‐binding of HDAC3 and Hs65K and subsequently reduced deacetylation of H3K9, illustrating a novel and conserved coupling mechanism that links the histone deacetylation with minor spliceosome for the regulation of gene expression.

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