Affinage

KHDRBS3

KH domain-containing, RNA-binding, signal transduction-associated protein 3 · UniProt O75525

Length
346 aa
Mass
38.8 kDa
Annotated
2026-04-28
68 papers in source corpus 23 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KHDRBS3 (T-STAR/SLM-2) is a STAR-family RNA-binding protein that functions as a concentration-dependent splicing repressor in the brain and regulates mRNA stability in diverse tissues. It homodimerizes through an unusual interface to achieve high-affinity binding to bipartite U(U/A)AA-repeat RNA motifs, and this dimerization is essential for its splicing-regulatory activity on key neuronal targets including Neurexin1-3 AS4 exons, where the density of UWAA binding sites determines paralog specificity between KHDRBS3 and SAM68 (PMID:26758068, PMID:27994030, PMID:23637638). Loss of KHDRBS3 in mice impairs cortical neural network activity, synapse formation, and causes behavioral deficits including anxiety and impaired novel object recognition (PMID:28009295, PMID:34196888). KHDRBS3 RNA-binding activity is negatively regulated by BRK/Sik tyrosine phosphorylation, and its protein stability is controlled by SIAH1/2 E3 ubiquitin ligase-mediated proteasomal degradation; in cancer contexts, KHDRBS3 regulates CD44 variant splicing to promote stemness and drug resistance, and stabilizes mRNAs encoding YWHAZ, EZH2, and ULK1 (PMID:15471878, PMID:15163637, PMID:33046798, PMID:37848941).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1999 High

    Identification of KHDRBS3 as a STAR-family RNA-binding protein related to SAM68 established its domain architecture and revealed that, unlike SLM-1, it is not a substrate for Src/Fyn kinases and does not engage canonical SH3-domain signaling partners, positioning it as a functionally distinct paralog.

    Evidence Biochemical kinase assays, SH2/SH3 pulldowns, yeast two-hybrid with testis cDNA, GFP localization in HeLa cells

    PMID:10077576 PMID:10332027

    Open questions at the time
    • Endogenous signaling partners in vivo not defined
    • Nuclear subcompartment identity (adjacent to nucleolus) not characterized
  2. 2001 Medium

    Demonstrating that KHDRBS3 overexpression inhibits colony formation in an RNA-binding domain–dependent manner linked its RNA-binding activity to a growth-suppressive function, raising the question of which RNA targets mediate this effect.

    Evidence Overexpression and RNA-binding domain deletion mutant in SV40-immortalized fibroblasts, colony formation assay

    PMID:11714634

    Open questions at the time
    • Target mRNAs mediating growth inhibition not identified
    • Mechanism of growth suppression (splicing, stability, or translational) unknown
    • Not replicated in non-immortalized cells
  3. 2004 High

    Two independent regulatory layers controlling KHDRBS3 activity were established: BRK/Sik tyrosine phosphorylation inhibits its RNA-binding capacity, while SIAH1/2-mediated ubiquitination targets it for proteasomal degradation, with the latter directly modulating its splicing-regulatory output.

    Evidence In vitro kinase assays with RNA-binding readout; yeast two-hybrid, Co-IP, minigene splicing assay, proteasome inhibitor rescue

    PMID:15163637 PMID:15471878

    Open questions at the time
    • Physiological contexts triggering BRK-mediated phosphorylation not defined
    • Whether SIAH regulation operates in brain tissue unclear (rodent SIAH site divergent)
    • Tyrosine residue(s) targeted by BRK on KHDRBS3 not mapped
  4. 2009 High

    SELEX-based identification of U(U/A)AA bipartite repeat motifs as the high-affinity RNA target defined the cis-regulatory code for KHDRBS3, explaining how it selects its pre-mRNA substrates.

    Evidence In vitro SELEX with purified protein, binding affinity validation

    PMID:19457263

    Open questions at the time
    • In vivo transcriptome-wide binding map not yet established at this point
    • Structural basis for bipartite recognition not yet resolved
  5. 2013 High

    Knockout mouse transcriptomics established KHDRBS3 as a physiological splicing repressor of Neurexin1-3 AS4 exons and Stxbp5l exon 23 in the brain, with splicing repression correlating with regional protein concentration and SAM68 unable to compensate, resolving the key in vivo targets.

    Evidence T-STAR null mouse, transcriptome-wide RNA-seq, minigene splicing assay, RT-PCR, response element mutagenesis

    PMID:23637638

    Open questions at the time
    • Downstream functional consequences of Neurexin AS4 mis-splicing not yet tested
    • Whether splicing changes cause behavioral deficits not yet assessed
  6. 2016 High

    Structural determination revealed that KHDRBS3 dimerizes through a non-canonical interface, and disrupting this interface abolishes both high-affinity RNA binding and splicing activity, establishing dimerization as essential for function; concurrently, a second knockout study showed that Slm2 loss reduces cortical network activity and causes anxiety and impaired cognition.

    Evidence Crystal structure, NMR, dimerization-interface mutagenesis, splicing reporter; Slm2-null mouse with RNA-seq, multi-electrode array, behavioral testing

    PMID:26758068 PMID:28009295

    Open questions at the time
    • How dimerization is regulated in vivo unknown
    • Whether behavioral phenotype maps to specific splice targets (e.g., Neurexins vs. Tomosyn2) not resolved
  7. 2017 High

    Domain-swap and binding-site-number experiments demonstrated that paralog specificity between KHDRBS3 and SAM68 on Neurexin2 AS4 is dictated by UWAA site density rather than differential protein-RNA contacts, establishing a quantitative model for target discrimination.

    Evidence Domain-swap mutagenesis, binding-site duplication, splicing reporters, in vivo cortex RNA binding

    PMID:27994030

    Open questions at the time
    • Structural basis for the STAR-domain region that confers paralog discrimination not resolved
    • Genome-wide application of the density model not tested
  8. 2018 Medium

    Extension of KHDRBS3 splicing regulation to cancer contexts showed that it controls CD44 variant splicing downstream of SALL4, producing CD44v isoforms that promote stemness and drug resistance in breast, gastric, and colorectal cancers.

    Evidence shRNA/siRNA knockdown, overexpression, sphere/organoid formation, CD44 splicing analysis, xenograft models

    PMID:29356399 PMID:33046798 PMID:33423358

    Open questions at the time
    • Whether CD44 is a direct KHDRBS3 splicing target (via UWAA motifs) or indirect not biochemically confirmed
    • Relative contribution of CD44v versus other splice targets to stemness phenotype unknown
  9. 2021 Medium

    KHDRBS3 was shown to function in the heart, binding sarcomere-encoding mRNAs and regulating titin alternative splicing and intron retention in dilated cardiomyopathy, and in neurons where its knockdown weakens LRRTM2-induced synapse formation by altering Neurexin AS4 splicing.

    Evidence CLIP-seq/RNA-seq in human heart tissue; shRNA knockdown in cerebellar neurons with artificial synapse formation assay

    PMID:34196888 PMID:34273561

    Open questions at the time
    • Causality between KHDRBS3 dysregulation and cardiomyopathy not established
    • Whether cardiac splicing targets use canonical UWAA motifs not assessed
  10. 2023 Medium

    Beyond splicing, KHDRBS3 was established as an mRNA stability regulator: it binds and stabilizes YWHAZ and EZH2 mRNAs to promote glycolysis and cell proliferation, respectively, and cooperates with circFOXP1-encoded protein p196 to stabilize ULK1 mRNA and activate autophagy in hepatocellular carcinoma.

    Evidence RNA pull-down, RIP, mRNA stability assays, functional epistasis with knockdown/overexpression, xenograft models

    PMID:36998321 PMID:37848941 PMID:40292405

    Open questions at the time
    • Mechanism by which KHDRBS3 stabilizes mRNA (e.g., competition with decay factors) not defined
    • Whether mRNA stabilization requires dimerization not tested
    • Single-lab findings for each target, not independently replicated

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis for KHDRBS3's mRNA stabilization function versus its splicing repression function; whether its cardiac splicing targets are causative in cardiomyopathy; and how post-translational modifications (BRK phosphorylation, SIAH ubiquitination) are regulated in physiological and disease contexts in vivo.
  • No in vivo CLIP-seq map in brain to comprehensively define direct targets
  • No structural model for mRNA stabilization mode
  • Functional relationship between splicing and mRNA stability activities unexplored

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 10 GO:0098772 molecular function regulator activity 5 GO:0140098 catalytic activity, acting on RNA 5
Localization
GO:0005634 nucleus 2 GO:0005654 nucleoplasm 1
Pathway
R-HSA-8953854 Metabolism of RNA 7 R-HSA-1643685 Disease 5 R-HSA-112316 Neuronal System 3 R-HSA-392499 Metabolism of proteins 1 R-HSA-9612973 Autophagy 1
Partners
KHDRBS1MTDHPTK6RBMY1A1SERPINB5SIAH1SIAH2
Complex memberships
T-STAR/SLM-2 homodimer

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 T-STAR/ETOILE (KHDRBS3) is an RNA-binding protein closely related to SAM68 that physically interacts with RBM (an RNA-binding protein encoded on the Y chromosome implicated in spermatogenesis), identified by yeast two-hybrid screen with testis cDNA. T-STAR/ETOILE fused with GFP accumulates in a novel nuclear compartment adjacent to the nucleolus when transfected into HeLa cells. Yeast two-hybrid screen, GFP transfection/live imaging Human molecular genetics Medium 10332027
1999 SLM-2 (KHDRBS3) is an RNA-binding protein containing a GSG/STAR domain with ~70% sequence identity to SAM68. Unlike SLM-1, SLM-2 is not tyrosine phosphorylated by Src or p59(fyn), and does not associate with SH3 domains of p59(fyn), Grb-2, PLCγ-1, or p120(rasGAP), distinguishing it functionally from SLM-1 as a signaling adapter. In vitro kinase assay, SH2/SH3 domain pulldown, RNA-binding assay Proceedings of the National Academy of Sciences of the United States of America High 10077576
2004 The nuclear tyrosine kinase BRK/Sik phosphorylates SLM-1 and SLM-2 (KHDRBS3), and this phosphorylation inhibits their RNA-binding activities. Active BRK/Sik expression increases nuclear retention of BRK/Sik itself. In vitro kinase assay, RNA-binding assay, mutagenesis, co-expression in cells The Journal of biological chemistry High 15471878
2004 T-STAR (KHDRBS3) is targeted for proteasome-dependent degradation by the E3 ubiquitin ligases SIAH1 and SIAH2, which bind to an octapeptide sequence in human T-STAR. This SIAH-mediated degradation modulates T-STAR-dependent alternative splicing activity. Rodent T-STAR orthologues are not targeted by SIAH1 due to sequence divergence at the binding site. Yeast two-hybrid, co-immunoprecipitation, minigene splicing assay, Western blot, proteasome inhibitor treatment Human molecular genetics High 15163637
2009 SLM-2 (KHDRBS3) binds RNA via direct U(U/A)AA repeat bipartite motifs identified by SELEX. The bipartite nature of the consensus sequence is essential for high-affinity RNA binding by SLM-2. SELEX (Systematic Evolution of Ligands by EXponential enrichment), in vitro RNA binding assay BMC molecular biology High 19457263
2011 SerpinB5 physically interacts with KHDRBS3 in gastric cancer cells, confirmed by co-immunoprecipitation. KHDRBS3 in turn interacts with FBXO32 mRNA, as demonstrated by RNA co-immunoprecipitation assay. KHDRBS3 is primarily detected in the nucleus of normal mucosal cells. Yeast two-hybrid, co-immunoprecipitation, RNA co-immunoprecipitation, Western blot, immunohistochemistry Oncology reports Medium 21725612
2013 T-STAR (KHDRBS3) functions as a potent splicing repressor of the alternatively spliced segment 4 (AS4) exons from Neurexin1-3 genes and exon 23 of Stxbp5l, identified by transcriptome-wide splicing analysis in T-STAR null mice. T-STAR regulates Neurexin2 AS4 through a UWAA-rich response element immediately downstream of the regulated exon. T-STAR protein concentration in forebrain-derived structures like hippocampus correlates with degree of Nrxn1-3 AS4 splicing repression. In the absence of T-STAR, Sam68 cannot compensate for Nrxn2 AS4 repression despite co-expression. T-STAR null mouse model, transcriptome-wide RNA-seq, minigene transfection splicing assay, RT-PCR, mutational analysis of response element PLoS genetics High 23637638
2016 T-STAR and Sam68 STAR proteins dimerize through an unexpected dimerization interface, and this dimerization is crucial for their biological activity in alternative splicing regulation. Crystal/NMR structure established atomic-resolution RNA binding mode; dimer formation increases RNA affinity and enables functional target selection within the transcriptome. Crystal structure, NMR, mutagenesis of dimerization interface, RNA binding assay, splicing reporter assay Nature communications High 26758068
2016 SLM2 (KHDRBS3) controls alternative splicing of Tomosyn2, LysoPLD/ATX, Dgkb, Kif21a, and Cask in addition to Neurexin1-3 AS4. SLM2 levels are maintained by a homeostatic feedback auto-regulation pathway. Loss of SLM2 decreases cortical neural network activity dependent on synaptic connections between SLM2-expressing pyramidal neurons and interneurons, and Slm2-null mice show anxiety and impaired novel object recognition. Slm2-null mouse, RNA-seq splicing analysis, multi-electrode array cortical network activity recording, behavioral testing Cell reports High 28009295
2017 The density of shared RNA binding sites (UWAA repeats) around a target exon, rather than different paralog-specific protein-RNA contacts, determines functional specificity between SLM2 (KHDRBS3) and Sam68 on the Neurexin2 AS4 exon. Doubling binding site numbers switched paralog sensitivity. Protein domain-swap experiments identified a region including the STAR domain that differentiates SLM2 and Sam68 splicing activity. Domain-swap mutagenesis, binding site mutagenesis/addition, splicing reporter assay, in vivo cortex RNA binding analysis Nucleic acids research High 27994030
2018 SALL4 upregulates KHDRBS3 expression, and KHDRBS3 in turn modulates CD44 alternative splicing, producing a CD44 variant (CD44v) lacking exons 8 and 9 that promotes cancer stemness (sphere formation, anoikis resistance) in basal-like breast cancer cells. shRNA knockdown, gene overexpression, sphere formation assay, splicing analysis, anoikis resistance assay Cancer medicine Medium 29356399
2019 Metadherin interacts with T-STAR (KHDRBS3) and Sam68, demonstrated by yeast two-hybrid and immunoprecipitation. Metadherin influences splice site selection in a dose-dependent manner in CD44v5-luc minigene reporter assays, and T-STAR is significantly overexpressed in prostate cancer tissue compared to benign prostate. Yeast two-hybrid, co-immunoprecipitation, CD44v5-luc minigene splicing reporter assay, immunohistochemistry Cancers Medium 31450747
2019 KHDRBS3 binds to circular RNA cDENND4C and increases its stability in glioma endothelial cells (GECs). The KHDRBS3/cDENND4C/miR-577 regulatory axis controls blood-tumor barrier permeability by modulating tight junction proteins ZO-1, occludin, and claudin-1. RNA immunoprecipitation, RNA stability assay, knockdown/overexpression, tight junction protein Western blot, BTB permeability assay Cell death & disease Medium 31296839
2020 KHDRBS3 promotes cancer stem cell-like features in gastric cancer organoids by regulating CD44 variant expression, contributing to 5-FU resistance and multi-drug resistance. KHDRBS3 was identified as a splicing regulator of CD44 variants in this cancer context. Organoid culture, 5-FU resistance induction, microarray, siRNA knockdown, CD44 variant splicing analysis Oncogene Medium 33046798
2021 SLM2 (KHDRBS3) binds to mRNAs encoding sarcomere constituents (MYL2, TNNI3, TNNT2, TPM1/2, TTN) in the human heart. Mechanistically, SLM2 mediates intron retention, prevents exon exclusion, and promotes alternative splicing of mRNA regions encoding the PEVK domain and I-band region of titin in dilated cardiomyopathy. RNA-seq in human heart, CLIP-seq/RNA immunoprecipitation, alternative splicing analysis, tissue-enrichment analysis Genomics, proteomics & bioinformatics Medium 34273561
2021 KHDRBS3 promotes drug resistance and anchorage-independent growth in colorectal cancer by regulating CD44 variant expression and the Wnt signaling pathway. KHDRBS3-positive cells show efficient tumor formation and lung metastasis in immunodeficient mice. siRNA knockdown, organoid formation, spheroid assay, xenograft mouse model, CD44 splicing analysis, Wnt pathway analysis Cancer science Medium 33423358
2021 SLM2 (KHDRBS3) knockdown in neurons reduces NRX AS4(-) isoform expression and weakens LRRTM2-induced synapse formation in cerebellar cultures. SLM2 modifies network formation in VIP-positive GABAergic interneurons through regulation of Nrxn splicing. shRNA knockdown in neurons, artificial synapse formation assay, immunostaining, RT-PCR for AS4 isoforms Neurochemical research Medium 34196888
2022 KHDRBS3 interacts with lncRNA MIR17HG in epithelial ovarian cancer cells. Overexpression of KHDRBS3 promotes glycolysis and paclitaxel resistance, effects rescued by MIR17HG overexpression. MIR17HG negatively regulates CLDN6 by binding its 3'UTR, defining a KHDRBS3-MIR17HG-CLDN6 regulatory axis. RNA immunoprecipitation, MTT assay, colony formation, seahorse glycolysis assay, xenograft model, 3'UTR reporter assay Life sciences Medium 35051418
2023 KHDRBS3 physically binds to YWHAZ mRNA (encoding 14-3-3ζ) as demonstrated by RNA pull-down and RNA immunoprecipitation assays, thereby upregulating 14-3-3ζ protein expression and promoting glycolysis and malignant progression in hepatocellular carcinoma. Silencing 14-3-3ζ reverses the pro-tumorigenic effects of KHDRBS3 overexpression. RNA pull-down, RNA immunoprecipitation, lentiviral knockdown/overexpression, xenograft model, seahorse glycolysis assay Cancer cell international Medium 37848941
2023 KHDRBS3 interacts with circHECTD1 (as shown by RIP and RNA pull-down), enhancing EZH2 mRNA stability and increasing EZH2 protein levels, thereby promoting proliferation and migration of brain vascular smooth muscle cells. RIP, RNA pull-down, qRT-PCR, knockdown/overexpression, CCK8, transwell assays Journal of inflammation research Medium 36998321
2025 circFOXP1-encoded protein p196 directly binds KHDRBS3 through its D2 domain (shown by Co-IP and RNA pull-down), forming a complex that stabilizes ULK1 mRNA, increasing ULK1 protein levels and activating autophagy to accelerate hepatocellular carcinoma progression. Co-immunoprecipitation, RNA pull-down, RIP, in vitro binding assay, loss/gain-of-function, xenograft International journal of nanomedicine Medium 40292405
2001 T-STAR (KHDRBS3) functions as a growth inhibitor; overexpression in SV40-transformed immortalized human fibroblasts strongly reduces colony formation, and deletion of the RNA-binding domain abrogates this growth-inhibitory effect. T-STAR is downregulated in immortalized cells that arose after proliferative crisis. mRNA differential display, overexpression with RNA-binding domain deletion mutant, colony formation assay Cell growth & differentiation Medium 11714634
2009 Mouse T-STAR (KHDRBS3) directly binds Fabp9 mRNA through sequences in its coding region and 3'UTR, identified from testis extract using SNAAP (isolation of specific nucleic acids associated with proteins). This suggests T-STAR regulates metabolism and expression of Fabp9 in spermatogenesis. SNAAP method (protein-mRNA pulldown from testis extract), direct binding assay Biochemistry. Biokhimiia Low 19916944

Source papers

Stage 0 corpus · 68 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Plasma membrane recruitment and activation of the AGC kinase Ypk1 is mediated by target of rapamycin complex 2 (TORC2) and its effector proteins Slm1 and Slm2. Proceedings of the National Academy of Sciences of the United States of America 116 22307609
2006 The phosphatidylinositol 4,5-biphosphate and TORC2 binding proteins Slm1 and Slm2 function in sphingolipid regulation. Molecular and cellular biology 116 16847337
2005 The pleckstrin homology domain proteins Slm1 and Slm2 are required for actin cytoskeleton organization in yeast and bind phosphatidylinositol-4,5-bisphosphate and TORC2. Molecular biology of the cell 111 15689497
1999 T-STAR/ETOILE: a novel relative of SAM68 that interacts with an RNA-binding protein implicated in spermatogenesis. Human molecular genetics 97 10332027
2006 Slm1 and slm2 are novel substrates of the calcineurin phosphatase required for heat stress-induced endocytosis of the yeast uracil permease. Molecular and cellular biology 89 16738335
1999 Characterization of Sam68-like mammalian proteins SLM-1 and SLM-2: SLM-1 is a Src substrate during mitosis. Proceedings of the National Academy of Sciences of the United States of America 89 10077576
2009 Amplification and overexpression of Hsa-miR-30b, Hsa-miR-30d and KHDRBS3 at 8q24.22-q24.23 in medulloblastoma. PloS one 79 19584924
2013 The tissue-specific RNA binding protein T-STAR controls regional splicing patterns of neurexin pre-mRNAs in the brain. PLoS genetics 72 23637638
2004 The nuclear tyrosine kinase BRK/Sik phosphorylates and inhibits the RNA-binding activities of the Sam68-like mammalian proteins SLM-1 and SLM-2. The Journal of biological chemistry 72 15471878
2006 The yeast PH domain proteins Slm1 and Slm2 are targets of sphingolipid signaling during the response to heat stress. Molecular and cellular biology 67 17101780
2009 The STAR RNA binding proteins GLD-1, QKI, SAM68 and SLM-2 bind bipartite RNA motifs. BMC molecular biology 66 19457263
2016 Structural basis of RNA recognition and dimerization by the STAR proteins T-STAR and Sam68. Nature communications 59 26758068
2021 Isolation and Characterization of a Novel Salmonella Phage vB_SalP_TR2. Frontiers in microbiology 55 34234757
2020 Molecular biological analysis of 5-FU-resistant gastric cancer organoids; KHDRBS3 contributes to the attainment of features of cancer stem cell. Oncogene 52 33046798
2004 SIAH1 targets the alternative splicing factor T-STAR for degradation by the proteasome. Human molecular genetics 44 15163637
2019 The Oncogene Metadherin Interacts with the Known Splicing Proteins YTHDC1, Sam68 and T-STAR and Plays a Novel Role in Alternative mRNA Splicing. Cancers 40 31450747
2018 SALL4 - KHDRBS3 network enhances stemness by modulating CD44 splicing in basal-like breast cancer. Cancer medicine 40 29356399
2019 KHDRBS3 regulates the permeability of blood-tumor barrier via cDENND4C/miR-577 axis. Cell death & disease 35 31296839
2011 ETOILE regulates developmental patterning in the filamentous brown alga Ectocarpus siliculosus. The Plant cell 35 21478443
2012 Plasma membrane proteins Slm1 and Slm2 mediate activation of the AGC kinase Ypk1 by TORC2 and sphingolipids in S. cerevisiae. Cell cycle (Georgetown, Tex.) 31 22895050
2022 KHDRBS3 promotes paclitaxel resistance and induces glycolysis through modulated MIR17HG/CLDN6 signaling in epithelial ovarian cancer. Life sciences 28 35051418
2022 Isolation and identification of the broad-spectrum high-efficiency phage vB_SalP_LDW16 and its therapeutic application in chickens. BMC veterinary research 25 36329508
2016 A SLM2 Feedback Pathway Controls Cortical Network Activity and Mouse Behavior. Cell reports 22 28009295
2018 SALP, a new single-stranded DNA library preparation method especially useful for the high-throughput characterization of chromatin openness states. BMC genomics 21 29439663
2011 SerpinB5 interacts with KHDRBS3 and FBXO32 in gastric cancer cells. Oncology reports 21 21725612
2005 Expression of the floral B-function gene SLM2 in female flowers of Silene latifolia infected with the smut fungus Microbotryum violaceum. Plant & cell physiology 21 15755743
2021 KHDRBS3 promotes multi-drug resistance and anchorage-independent growth in colorectal cancer. Cancer science 19 33423358
2020 Finding new cancer epigenetic and genetic biomarkers from cell-free DNA by combining SALP-seq and machine learning. Computational and structural biotechnology journal 19 32774784
2017 Binding site density enables paralog-specific activity of SLM2 and Sam68 proteins in Neurexin2 AS4 splicing control. Nucleic acids research 16 27994030
2016 Rapid Evolutionary Rates and Unique Genomic Signatures Discovered in the First Reference Genome for the Southern Ocean Salp, Salpa thompsoni (Urochordata, Thaliacea). Genome biology and evolution 16 27624472
2010 Higher HIV-1 DNA associated with lower gains in CD4 cell count among patients with advanced therapeutic failure receiving optimized treatment (ANRS 123--ETOILE). The Journal of antimicrobial chemotherapy 15 20667886
2021 SLM2 Is A Novel Cardiac Splicing Factor Involved in Heart Failure due to Dilated Cardiomyopathy. Genomics, proteomics & bioinformatics 14 34273561
2019 Antibacterial action of synthetic antilipopolysaccharide peptides (SALP) involves neutralization of both membrane-bound and free toxins. The FEBS journal 12 30843356
2019 Decoding genetic and epigenetic information embedded in cell free DNA with adapted SALP-seq. International journal of cancer 11 30746694
2006 Expression of T-STAR gene is associated with regulation of telomerase activity in human colon cancer cell line HCT-116. World journal of gastroenterology 11 16810759
2001 Down-regulation of T-STAR, a growth inhibitory protein, after SV40-mediated immortalization. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 11 11714634
2023 KHDRBS3 accelerates glycolysis and promotes malignancy of hepatocellular carcinoma via upregulating 14-3-3ζ. Cancer cell international 9 37848941
2025 BIMSSA: enhancing cancer prediction with salp swarm optimization and ensemble machine learning approaches. Frontiers in genetics 8 39834551
2010 Expression and functions of the star proteins Sam68 and T-STAR in mammalian spermatogenesis. Advances in experimental medicine and biology 8 21189686
2025 Exosome-Delivered circFOXP1 Upregulates Autophagy and Promotes Hepatocellular Carcinoma Progression Through Its Encoded p196 Protein Targeting the KHDRBS3/ULK1 Axis. International journal of nanomedicine 7 40292405
2001 T-STAR gene: fine mapping in the candidate region for childhood absence epilepsy on 8q24 and mutational analysis in patients. Epilepsy research 7 11463515
2011 Space-time decoupling in the branching process in the mutant étoile of the filamentous brown alga Ectocarpus siliculosus. Plant signaling & behavior 6 22095146
2000 Intravenous administration of stabilized antisense lipid particles (SALP) leads to activation and expansion of liver natural killer cells. Antisense & nucleic acid drug development 6 10905558
2021 Distinct Expression of SLM2 Underlies Splicing-Dependent Trans-Synaptic Signaling of Neurexin Across GABAergic Neuron Subtypes. Neurochemical research 5 34196888
2023 circHECTD1 Promotes the Proliferation and Migration of Human Brain Vascular Smooth Muscle Cells via Interacting with KHDRBS3 to Stabilize EZH2 mRNA Expression. Journal of inflammation research 4 36998321
2017 [Knock-down of KHDRBS3 gene inhibits proliferation of human ovarian cancer CAOV-3 cells]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 4 28871947
2009 Identification of messenger RNA substrates for mouse T-STAR. Biochemistry. Biokhimiia 4 19916944
2017 Neuroligin-induced presynaptic differentiation through SLM2-mediated splicing modifications of neurexin in cerebellar cultures. Biochemical and biophysical research communications 3 28939043
2025 Memetic Salp Swarm Algorithm for economic load dispatch problems. Scientific reports 2 40835728
2024 KHDRBS3 facilitates self-renewal and temozolomide resistance of glioblastoma cell lines. Life sciences 2 39413902
2018 Immunological response to bacterial infection in a pelagic tunicate: Inflammation in the salp Thalia democratica. Journal of invertebrate pathology 2 30359568
2003 [Association of child absence epilepsy with T-STAR gene]. Zhonghua yi xue za zhi 2 12921630
2026 Comparative embryogenesis of two salp species reveals rogue development and evolutionary divergence from sessile tunicates. PLoS biology 1 41843499
2024 Characterization and genomic analysis of Salmonella Abortusequi phage, vB_SalP_LDDK01, and its biocontrol application in donkey meat. Frontiers in cellular and infection microbiology 1 39764155
2020 Safety biomarkers for development of vaccines and biologics: Report from the safety biomarkers symposium held on November 28-29, 2017, Marcy l'Etoile, France. Vaccine 1 33187767
2018 Correction to: SALP, a new single-stranded DNA library preparation method especially useful for the high-throughput characterization of chromatin openness states. BMC genomics 1 29728049
2026 Macroid Formation in Salmacina stellaebayensis n. sp. From Mauritania's Baie de l'Étoile With New Insights on Mitogenome Evolution in Serpulidae (Annelida). Ecology and evolution 0 41624108
2026 Optimized Gene Selection Using Nomadic People and Salp Swarm Algorithms for Cancer Detection. IEEE transactions on computational biology and bioinformatics 0 42024922
2025 Integrated transcriptome analysis and in silico investigations identify KHDRBS3 to target with steroidal lactone in paclitaxel resistance breast cancer. Biochemical and biophysical research communications 0 40651363
2025 KHDRBS3-mediated upregulation of circ_0024107 in gastric cancer cells and GC-MSCs synergistically drives gastric cancer cell migration and invasion. In vitro cellular & developmental biology. Animal 0 40760232
2025 An Enhanced Knowledge Salp Swarm Algorithm for Solving the Numerical Optimization and Seed Classification Tasks. Biomimetics (Basel, Switzerland) 0 41002872
2025 Salp swarm-optimized machine learning models for predicting preoperative aortic rupture risk in acute type a aortic dissection patients. Frontiers in physiology 0 41245264
2025 Classification of coding and non-coding regions in eukaryotic gene sequences using an adaptive anti-notch filter designed using hybrid Salp SwarmWhale algorithm incorporating a modified error function. Computational biology and chemistry 0 41259968
2025 Roles of KHDRBS2 and KHDRBS3 in prostate cancer progression and AR-V7 regulation. Discover oncology 0 41417173
2025 Therapeutic efficacy of phage vB_SalP_NW15 and cinnamaldehyde against drug-resistant Salmonella Enteritidis in a chicken infection model. Poultry science 0 41485350
2024 Salp-J Colony Optimization-based advanced hybrid ensemble deep predictor with LSTM for protein structure prediction. Journal of biomolecular structure & dynamics 0 38444340
2022 An internet traffic classification method based on echo state network and improved salp swarm algorithm. PeerJ. Computer science 0 35494824
2022 Application of an improved Discrete Salp Swarm Algorithm to the wireless rechargeable sensor network problem. Frontiers in bioengineering and biotechnology 0 36204468