Dust Cover
- Known as:
- Dust Cover
- Catalog number:
- dia20dc015
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Diasource
- Gene target:
- Dust Cover
Related genes to: Dust Cover
- Gene:
- DSTYK NIH gene
- Name:
- dual serine/threonine and tyrosine protein kinase
- Previous symbol:
- RIPK5
- Synonyms:
- KIAA0472, DustyPK, RIP5
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-02
- Date modifiied:
- 2016-10-05
Related products to: Dust Cover
Related articles to: Dust Cover
- Thrombopoietin receptor agonists (TPO-RAs) represent a cornerstone in immune thrombocytopenia (ITP) management, yet their molecular mechanisms remain incompletely elucidated. This study systematically deciphered the key targets and signaling networks of four TPO-RAs (romiplostim, eltrombopag, avatrombopag, hetrombopag) in ITP pathogenesis. Network pharmacology was integrated with single-cell high-dimensional weighted gene co-expression network analysis (hdWGCNA) using bone marrow scRNA-seq data from ITP patients and healthy controls. Metacell-based co-expression modules to hematopoietic bone marrow cells were identified. Drug targets were curated from multiple databases, and candidate genes were screened by intersecting differentially expressed genes (DEGs), cell specific modules, and TPO-RA targets. Molecular docking, pseudotime trajectory analysis, and in silico gene knockdown were employed for functional validation. Intersection analysis revealed five key genes (CACNA1A, CSF1R, PKN1, CD9, DSTYK). Molecular docking demonstrated strong binding affinities between TPO-RAs and key targets. The ITP bone marrow niche exhibited rewired cell-cell communication, with enhanced T cell-initiated signaling and aberrant megakaryocyte-T cell interactions. Pseudotime analysis uncovered disrupted megakaryocyte maturation dynamics. In silico knockdown revealed CACNA1A, CSF1R, and PKN1 dysregulation exacerbated neutrophil hyperactivity, while CD9 and DSTYK knockdown impaired mitotic regulation. This study delineated mechanisms of TPO-RAs, highlighting five key genes that orchestrate dysregulated thrombopoiesis and immune dysfunction in ITP. The integration of in silico strategies identified novel targets for optimizing ITP therapy. - Source: PubMed
Publication date: 2026/04/01
Wang WanruWang HaoxuWan XiaohanCao JunyingWang RuixueHou Ming - Immunotherapy has transformed the treatment of non-small cell lung cancer (NSCLC). Yet, acquired resistance remains a major clinical challenge. Defining molecular determinants of tumor sensitivity to T cell-mediated killing is therefore critical. Tumor necrosis factor α (TNF-α) released by cytotoxic T cells promotes tumor cell death, whereas NF-κB signaling supports survival. Autophagy counteracts TNFα-induced apoptosis, and its inhibition enhances responses to immune checkpoint inhibitors (ICIs). Genomic alterations further contribute to immune evasion and reduced immunotherapy efficacy. We previously identified DSTYK, a dual serine/threonine and tyrosine kinase amplified in NSCLC, as a suppressor of TNF-α-mediated CD8 T cell killing and a driver of ICI resistance through autophagy. Here, we show that DSTYK modulates TNFR1 signaling by phosphorylating the autophagy initiator ULK1, which enables ULK1-dependent phosphorylation of RIPK1. Loss of DSTYK disrupts ULK1 activation, promotes RIPK1 autophosphorylation, proapoptotic signaling, and impaired NF-κB-dependent survival. These findings define a DSTYK-ULK1-RIPK1 axis controlling TNF-α-induced apoptosis and support targeting ULK1 to sensitize DSTYK-amplified NSCLC to T cell-mediated killing. - Source: PubMed
Publication date: 2026/03/12
Pasquier AndreaViu-Idocin CristinaArricibita AndreaEchepare MirariPicabea BeñatOrive DanielÁlava AneFernández-Irigoyen JoaquínSantamaría EnriqueArgueta AllanMolina EvaPineda-Lucena AntonioGentili MarcoFacchinetti FedericaRoz LucaMontuenga Luis MValencia Karmele - Hereditary spastic paraplegia (HSP) is a group of disorders that mostly affect the upper motor neurons of the spinal cord, with varying inheritance patterns and clinical presentations. We present the case of an 18-year-old male patient who was medically evaluated at a recruitment center due to non-specific complaints of joint pain and difficulty breathing over several years, without an established diagnosis or treatment. Physical examination revealed significant asymmetric muscle weakness in both legs and asymmetrical patellar reflexes. The patient was referred to diverse specialists and underwent a series of diagnostic tests, including blood work, serology, electromyography, nerve conduction tests, and magnetic resonance imaging of the brain and spine. No specific pathology related to the patient's symptoms was identified. Genetic testing, however, revealed heterozygous likely pathogenic variants in both (c.898-2A>G) and (c.1742T>C, p.Leu581Ser) genes, confirming the diagnosis of HSP. This case is notable for the rare occurrence of two distinct, very rare genetic mutations contributing to the pathogenesis of HSP, a situation called dual molecular diagnosis. We report a rare case of HSP dual molecular diagnosis. Both and act on membrane dynamics, critical in neuronal maintenance and axonal transport, essential processes disrupted in HSP. Further investigation is required to inform about potential interaction and the underlying molecular mechanism. Moreover, from the clinical perspective, the diagnostic workup brings to light the importance of awareness of a relatively rare disease and of thorough and comprehensive medical analysis to evaluate and rule out diverse potential causes. - Source: PubMed
Publication date: 2025/08/13
Machluf YossySaid MajdChechik YigalBen-Dor ShifraChaiter Yoram - Congenital scoliosis (CS), a severe form of early-onset scoliosis (EOS), arises from vertebral malformations during embryogenesis, driven by complex genetic and environmental interactions. This review synthesizes recent advances in understanding CS etiology, diagnosis, and treatment. Genetically, CS is linked to mutations in TBX6, GDF3, DSTYK, and COL11A2, alongside copy number variations (CNVs) and epigenetic modifications such as allele-specific methylation in SVIL and TNS3. Maternal hypoxia, toxin exposure, and nutritional deficiencies further contribute to pathogenesis. Diagnosis incorporates advanced imaging techniques-such as X-rays, magnetic resonance imaging (MRI), and computed tomography (CT)-as well as genetic testing, with whole-exome sequencing identifying mutations in 18.6% of cases. Conservative management, including casting and bracing (e.g., alternating cast and brace treatment [ARCBT] and 3D-printed orthoses), effectively delays progression in mild-to-moderate cases. Surgical interventions-such as hemivertebra resection, hybrid techniques (HT), and growth-modulating technologies including magnetic controlled growth rods (MCGR) and the Shilla method-have demonstrated improved outcomes in patients with severe deformities. HT combines posterior osteotomy with dual growing rods, achieving significant Cobb angle correction (81.4° to 40.1°) and spinal growth (1.23 cm/year) with fewer complications. MCGR reduces repeated surgeries but shows variable impacts on quality of life. Emerging approaches, including apical control techniques and robotics, highlight the shift toward personalized care. This review underscores the need for multidisciplinary strategies to optimize outcomes, emphasizing early diagnosis, tailored treatments, and long-term monitoring to address CS complexity. - Source: PubMed
Publication date: 2025/07/29
Peng ZhimingZhang HaoranWang ShengruZhang Jianguo - Prostatitis is a common condition in andrology and urology that significantly impacts the quality of life of affected individuals. Current treatments often fail to provide lasting benefits. To identify novel therapeutic targets, we conducted a drug-targeted Mendelian randomization (MR) study. Using cis-expression quantitative trait loci (cis-eQTL) data from the eQTLGen Consortium combined with Genome-Wide Association Studies (GWAS) data on prostatitis from FinnGen, we performed a two-sample MR analysis. This analysis identified nine potential causal genes: ANXA1, CRY2, DSTYK, FKBP1A, LAMA5, NENF, PTGIR, STK39, and TGFA. Following heterogeneity testing, horizontal pleiotropy assessment, and bidirectional MR, CRY2 and PTGIR were validated in the Genotype-Tissue Expression (GTEx) portal replication phase. Bayesian colocalization analysis and genetic correlation analysis investigations provided strong evidence of shared causal variants with prostatitis and negative genetic correlations for these genes. PheWAS indicated negligible horizontal pleiotropy, and drug prediction analysis identified potential targeting agents for CRY2 and PTGIR. This study highlights CRY2 and PTGIR as promising therapeutic targets for prostatitis, providing new insights into its genetic underpinnings and offering potential pathways for developing effective treatments. - Source: PubMed
Publication date: 2025/05/30
Yan KunTao YifangChen BohongZhang DongLi ZihaoLi CaogangZhang Peng