Last update 19 Sep 2024

KHDRBS3

Last update 19 Sep 2024

Basic Info

Synonyms

Etle, etoile, KH domain-containing, RNA-binding, signal transduction-associated protein 3

+ [9]

Introduction

RNA-binding protein that plays a role in the regulation of alternative splicing and influences mRNA splice site selection and exon inclusion. Binds preferentially to the 5'-[AU]UAAA-3' motif in vitro. Binds optimally to RNA containing 5'-[AU]UAA-3' as a bipartite motif spaced by more than 15 nucleotides. Binds poly(A). RNA-binding abilities are down-regulated by tyrosine kinase PTK6 (PubMed:10564820, PubMed:19561594, PubMed:26758068). Involved in splice site selection of vascular endothelial growth factor (PubMed:15901763). In vitro regulates CD44 alternative splicing by direct binding to purine-rich exonic enhancer (By similarity). Can regulate alternative splicing of neurexins NRXN1-3 in the laminin G-like domain 6 containing the evolutionary conserved neurexin alternative spliced segment 4 (AS4) involved in neurexin selective targeting to postsynaptic partners such as neuroligins and LRRTM family members (PubMed:26758068). Targeted, cell-type specific splicing regulation of NRXN1 at AS4 is involved in neuronal glutamatergic synapse function and plasticity (By similarity). May regulate expression of KHDRBS2/SLIM-1 in defined brain neuron populations by modifying its alternative splicing (By similarity). Can bind FABP9 mRNA (By similarity). May play a role as a negative regulator of cell growth. Inhibits cell proliferation. (Microbial infection) Involved in post-transcriptional regulation of HIV-1 gene expression.

100 Clinical Results associated with KHDRBS3

100 Translational Medicine associated with KHDRBS3

0 Patents (Medical) associated with KHDRBS3

162

Literatures (Medical) associated with KHDRBS3

01 Aug 2024·American Journal of Reproductive Immunology

Long non‐coding RNA TPT1‐AS1 inhibits ferroptosis in ovarian cancer by regulating GPX4 via CREB1 regulation

Article

Author: Chi, Xiaohong ; Bai, Xiaoying ; Wang, Yan ; Liu, Juanni ; Cao, Lei

AbstractBackgroundLong non‐coding RNAs (lncRNAs) play crucial roles in cellular processes, with dysregulation implicated in various diseases, including cancers. The lncRNA TPT1‐AS1 (TPT1 Antisense RNA 1) promotes tumor progression in several cancers, including ovarian cancer (OC), but its influence on ferroptosis and interaction with other proteins remains underexplored.MethodsIn this study, we employed a multi‐faceted approach to investigate the functional significance of TPT1‐AS1 in OC. We assessed TPT1‐AS1 expression in OC specimens and cell lines using RT‐qPCR, in situ hybridization (ISH), and fluorescence in situ hybridization (FISH) assays. Functional assays included evaluating the impact of TPT1‐AS1 knockdown on OC cell proliferation, migration, invasiveness, and cell cycle progression. Further, we explored and validated the interaction of TPT1‐AS1 with other proteins using bioinformatics. Finally, we investigated TPT1‐AS1 involvement in erastin‐induced ferroptosis using Iron Assay, Malondialdehyde (MDA) assay, and reactive oxygen species (ROS) detection.ResultsOur findings revealed that TPT1‐AS1 overexpression in OC correlated with an unfavorable prognosis. TPT1‐AS1 knockdown suppressed cell proliferation, migration, and invasiveness. Additionally, TPT1‐AS1 inhibited erastin‐induced ferroptosis, and in vivo experiments confirmed its oncogenic impact on tumor development. Mechanistically, TPT1‐AS1 was found to regulate Glutathione Peroxidase 4 (GPX4) transcription via CREB1 (cAMP response element‐binding protein 1) and interact with RNA‐binding protein (RBP) KHDRBS3 (KH RNA Binding Domain Containing, Signal Transduction Associated 3) to regulate CREB1.ConclusionTPT1‐AS1 promotes OC progression by inhibiting ferroptosis and upregulating CREB1, forming a regulatory axis with KHDRBS3. These findings highlight the regulatory network involving lncRNAs, RBPs, and transcription factors in cancer progression.

17 May 2024·Science Advances

Spinning and corkscrewing of oceanic macroplankton revealed through in situ imaging

Article

Author: Damian-Serrano, Alejandro ; Du Clos, Kevin T ; Sutherland, Kelly R ; Colin, Sean P ; Costello, John H ; Gemmell, Brad J

Helical motion is prevalent in nature and has been shown to confer stability and efficiency in microorganisms. However, the mechanics of helical locomotion in larger organisms (>1 centimeter) remain unknown. In the open ocean, we observed the chain forming salp, Iasis cylindrica , swimming in helices. Three-dimensional imaging showed that helicity derives from torque production by zooids oriented at an oblique orientation relative to the chain axis. Colonies can spin both clockwise and counterclockwise and longer chains (>10 zooids) transition from spinning around a linear axis to a helical swimming path. Propulsive jets are non-interacting and directed at a small angle relative to the axis of motion, thus maximizing thrust while minimizing destructive interactions. Our integrated approach reveals the biomechanical advantages of distributed propulsion and macroscale helical movement.

08 May 2024·Nucleic Acids Research

Differential expression of paralog RNA binding proteins establishes a dynamic splicing program required for normal cerebral cortex development

Article

Author: Sette, Claudio ; Pagliarini, Vittoria ; Cesari, Eleonora ; Naro, Chiara ; Orsini, Tiziana ; D'Amelio, Marcello ; Farini, Donatella ; Geloso, Maria Concetta ; La Barbera, Livia ; Elliott, David J ; Testa, Erika ; Tamagnone, Luca ; Viscomi, Maria Teresa ; Fort, Philippe ; Guerra, Marika ; Vecchioli, Stefano Farioli ; Medici, Vanessa ; Ehrmann, Ingrid

AbstractSam68 and SLM2 are paralog RNA binding proteins (RBPs) expressed in the cerebral cortex and display similar splicing activities. However, their relative functions during cortical development are unknown. We found that these RBPs exhibit an opposite expression pattern during development. Sam68 expression declines postnatally while SLM2 increases after birth, and this developmental pattern is reinforced by hierarchical control of Sam68 expression by SLM2. Analysis of Sam68:Slm2 double knockout (Sam68:Slm2dko) mice revealed hundreds of exons that respond to joint depletion of these proteins. Moreover, parallel analysis of single and double knockout cortices indicated that exons regulated mainly by SLM2 are characterized by a dynamic splicing pattern during development, whereas Sam68-dependent exons are spliced at relatively constant rates. Dynamic splicing of SLM2-sensitive exons is completely suppressed in the Sam68:Slm2dko developing cortex. Sam68:Slm2dko mice die perinatally with defects in neurogenesis and in neuronal differentiation, and develop a hydrocephalus, consistent with splicing alterations in genes related to these biological processes. Thus, our study reveals that developmental control of separate Sam68 and Slm2 paralog genes encoding homologous RBPs enables the orchestration of a dynamic splicing program needed for brain development and viability, while ensuring a robust redundant mechanism that supports proper cortical development.

News (Medical) associated with KHDRBS3

20 Jan 2023

·www.prnewswire.com

BriSTAR Immunotech To Present its Novel Cell Therapy for Acute Myeloid Leukemia at the AACR Special Conference on AML and MDS

TORONTO, Canada and BEIJING, Jan. 20, 2023 /PRNewswire/ -- BriSTAR Immunotech, a clinical-stage cell therapy company, announced today it will showcase its T-cell receptors (TCR) and antigen receptor (STAR)-T cell therapy technology platform at the American Association for Cancer Research (AACR) special conference on acute myeloid leukemia and myelodysplastic syndrome, taking place January 23-25, 2023, in Austin, Texas. "The data shows that our LILRB4 STAR-T cell therapy exhibits potent anti-tumor activity against AML in preclinical models," said Dr. James Pan, CEO at BriSTAR Immunotech. "These findings support our strategy to maximize the potential of our unique STAR-T technology platform." Presentation Details: Abstract title: Development of LILRB4 biparatopic synthetic T-cell receptor and antigen receptor (STAR)-T cells for the treatment of acute myeloid leukemia (AML) Presenter: Dr. James Pan Date / Time: Tuesday, January 24, 2023 7:15 - 9:30 p.m. CST The complete abstract will be available here. An electronic copy of the poster is available upon request EMAIL: [email protected]. About LILRB4 STAR-T BriSTAR Immunotech has developed LILRB4 STAR-T cell therapy for the treatment of relapsed/refractory acute myeloid leukemia (R/R AML). This novel cell therapy drug candidate was developed using BriSTAR's STAR-T platform to introduce the biparatopic STAR gene targeting LILRB4 into autologous T cells with a lentiviral gene transduction approach. This next generation T cell therapy uses two novel nano-antibodies that bind to different epitopes and fused to the alpha and beta chains of the STAR structure, respectively. This gives LILRB4 START-T better antigen engagement and increased cytotoxicity against this highly aggressive AML. In December 2022, the LILRB4 STAR-T program received Orphan Drug Designation from the U.S. FDA. About Acute Myeloid Leukemia (AML) Acute myeloid leukemia (AML) is a cancer of the blood and bone marrow. AML occurs when a bone marrow cell suddenly develops genetic abnormalities. It is highly heterogeneous with limited therapeutic options and poor prognosis. AML is the most common acute leukemia in adults, with an incidence of over 20 000 cases per year in the United States alone, and China ranked among the top three in the world in terms of the number of AML cases and deaths, with 13,200 and 7,100 cases, respectively. For patients with relapse/refractory AML, there is no treatment that significantly extends the survival period of 5-9 months. About STAR-T Platform BriSTAR Immunotech's synthetic TCR and antigen receptor (STAR)-T cell therapy technology platform is highly effective at building a product pipeline for both hematological and solid tumors. STAR-T has the characteristics of natural T cells, such as sensitive target engagement and strong tumor infiltration and offers a natural framework for engineering dual-targeting T cell products. In September 2022, an investigational new drug (IND) application for CD19/CD20 STAR-T cell injection (research code: HXYT-001) was granted by Center for Drug Evaluation (CDE), National Medical Products Administration (NMPA), for the treatment of recurrent/refractory non-Hodgkin lymphoma (B-NHL). In addition, the STAR-T exploratory clinical studies have been initiated for several types of solid tumors. About BriSTAR Immunotech BriSTAR Immunotech Ltd is a clinical-stage cell therapy company founded in 2018, focusing on developing better T cell therapies for the treatment of cancer and viral infections. The Company has two proprietary technology platforms, STAR-T and enTCR-T. STAR-T, like CAR-T is HLA-independent, but uses full TCR-signaling complex to engage and kill cancer cells. EnTCR-T engages a co-stimulatory signaling, in addition to the TCR complex, for clearing viral infections. Our current pipeline includes product candidates indicated for AML and solid tumors, as well as viral infections. Our lead product, a dual targeting CD19/CD20 STAR-T candidate, is currently in clinical trials for relapsed/refractory B-cell non-Hodgkin lymphoma (r/r B-NHL). SOURCE Bristar Immunotech Limited

Cell TherapyINDImmunotherapyClinical StudyOrphan Drug

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KHDRBS3

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