SRM™ 200 Dust Protective Cover
- Known as:
- SRM™ 200 Dust Protective Cover
- Catalog number:
- 1441
- Product Quantity:
- 1 each
- Category:
- -
- Supplier:
- Sakura
- Gene target:
- SRM™ 200 Dust Protective Cover
Related genes to: SRM™ 200 Dust Protective 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
- Gene:
- SRM NIH gene
- Name:
- spermidine synthase
- Previous symbol:
- SRML1
- Synonyms:
- SPS1
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-29
- Date modifiied:
- 2016-10-05
- Gene:
- SRMS NIH gene
- Name:
- src-related kinase lacking C-terminal regulatory tyrosine and N-terminal myristylation sites
- Previous symbol:
- C20orf148
- Synonyms:
- SRM, dJ697K14.1, PTK70
- Chromosome:
- 20q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-16
- Date modifiied:
- 2016-04-29
- Gene:
- SRRM1 NIH gene
- Name:
- serine and arginine repetitive matrix 1
- Previous symbol:
- -
- Synonyms:
- SRM160, POP101, MGC39488
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-24
- Date modifiied:
- 2016-10-05
Related products to: SRM™ 200 Dust Protective Cover
'VX-200 Vortex Mixer Optional head attachment for 1 microplate or 64 x 0.2 ml tubes or 8 x 0.2 ml tube strips'VX-200 Vortex Mixer Optional head attachment for 12 x 1.5/2.0 ml tubes, held horizontally'VX-200 Vortex Mixer Optional head attachment for 2 x 50 ml tubes, held horizontally'VX-200 Vortex Mixer Optional head attachment for 24 x 1.5/2.0 ml tubes, 24 x 0.5 ml tubes and 32 x 0.2 ml tubes (or 4 tube strips)'VX-200 Vortex Mixer Optional head attachment for 4 x 15 ml tubes, held horizontally'VX-200 Vortex Mixer Optional head attachment for 6 x 50 ml tubes'VX-200 Vortex Mixer Optional head attachment for 8 x 15 ml and 8 x 12/13 mm diameter tubes(R)-Bicalutamide0.02 M Iodine in THF _ pyridine _ water
(V _ V _ V = 70 _ 20 _ 10), Oxidization0.02 M Iodine in THF _ pyridine _ water
(V _ V _ V = 89.6 _ 0.4 _ 10), Oxidization0.3 M Hyacinth BMT Solution in anhydrous acetonitrile with 0.5% NMI
purity >98%, <20 ppm water, Activators0.5 - 10ul pipette tips, extended length, case of 19,200 racked tips (supplied in 20 packs containing 10 x 96 racks)0.5 - 10ul pipette tips, extended length, case of 19,200 racked tips (supplied in 5 packs containing 10 x 96 racks)0.5 _ 10ul pipette tips, extended length, case of 19,200 racked tips (supplied in 20 packs containing 10 x 96 racks)1 kb DNA Ladder 500 _ 10,200 bp Related articles to: SRM™ 200 Dust Protective Cover
- Patient-derived xenograft (PDX) models are widely regarded as robust preclinical platforms because they preserve the histopathological and molecular features of primary tumors. In this study, we established twenty triple-negative breast cancer (TNBC) PDX models using freshly resected patient tumors, including ten with high DSTYK expression and ten with low DSTYK expression. Tumor fragments were orthotopically implanted into the fourth mammary fat pads of NSG mice. DSTYK expression was validated by immunohistochemistry and western blotting. Histological evaluation across three serial passages demonstrated that PDX tumors retained the cellular morphology, stromal architecture, and lineage characteristics of their corresponding primary tumors. Using these models, we assessed responses to combination chemotherapy with doxorubicin and docetaxel. DSTYK-low PDX tumors exhibited significantly greater chemosensitivity, whereas DSTYK-high tumors showed marked resistance, indicating a critical role for DSTYK in mediating chemotherapy resistance. Consistent with these findings, analyses from The Human Protein Atlas and Kaplan-Meier Plotter databases revealed that high DSTYK expression is associated with poor survival outcomes in TNBC patients. Collectively, our results from clinical specimens, PDX models, and public datasets identify DSTYK as a promising prognostic biomarker and predictor of chemotherapeutic response in TNBC, with potential implications for patient stratification and treatment optimization. - Source: PubMed
Publication date: 2026/05/07
Rojas SamuelZhang JinyuElam Brianna MSchwarz GenevieveZou YueJiang Yong - Although aldehyde dehydrogenases 1 family member A1 (ALDH1A1) has been extensively studied in cancer, its role in hepatocellular carcinoma (HCC) remains poorly understood. This study was designed to characterize the expression pattern and functional roles of ALDH1A1 in HCC, and to further investigate its underlying molecular mechanisms using integrated proteomic analysis. - Source: PubMed
Yue HanxunHu ZenanWu GuozhiLi RenpengJiang N AZheng Y AWang YupingZhou Yongning - 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