BOTTLE,BOD,300ML,STOPPER,NUMBERS 25_48
- Known as:
- BOTTLE,BOD,300ML,STOPPER,NUMBERS 25_48
- Catalog number:
- 15070-25
- Product Quantity:
- 24
- Category:
- -
- Supplier:
- Kimb
- Gene target:
- BOTTLE BOD 300ML STOPPER NUMBERS 25_48
Related genes to: BOTTLE,BOD,300ML,STOPPER,NUMBERS 25_48
- Gene:
- KXD1 NIH gene
- Name:
- KxDL motif containing 1
- Previous symbol:
- C19orf50
- Synonyms:
- FLJ25480, MGC2749, KXDL, BORCS4
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-08
- Date modifiied:
- 2015-08-07
- Gene:
- RAB3IP NIH gene
- Name:
- RAB3A interacting protein
- Previous symbol:
- -
- Synonyms:
- RABIN3, FLJ22548, RABIN8
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-12
- Date modifiied:
- 2015-08-25
Related products to: BOTTLE,BOD,300ML,STOPPER,NUMBERS 25_48
Related articles to: BOTTLE,BOD,300ML,STOPPER,NUMBERS 25_48
- Bladder cancer (BC) is a prevalent malignant tumor worldwide, posing a significant public health burden and challenge to human society. Current therapeutic modalities for BC include surgical treatment, radiotherapy, chemotherapy, targeted therapy, and immunosuppressive therapy. However, almost all patients experience disease progression and ultimately succumb to BC. Our study demonstrated that elevated expression of Heat Shock Protein Beta-6 (HSPB6) correlated with higher clinical grades and stages, establishing it as an independent prognostic risk factor for BC. Enrichment analysis indicated that HSPB6 is associated with the extracellular matrix in BC. Experimental validation revealed that HSPB6 overexpression inhibits the proliferation of BC cell line T24. This effect may be achieved by inhibiting the PI3K/Akt signaling pathway, which in turn leads to inhibition of epithelial-mesenchymal transition (EMT). Furthermore, we developed a prognostic risk model that incorporated DDR2, DPYSL3, MFAP5, PDGFRB, and SPOCD1, allowing accurate prediction of patient outcomes based on immunological status. In conclusion, this study highlights that HSPB6 overexpression can restrain the proliferation of BC cells and inhibit EMT, underscoring its potential as a diagnostic marker and therapeutic target in BC. - Source: PubMed
Publication date: 2026/04/20
Wang Jian-SheQiu Yi-FanZhang LuJi BoLiang SenWang Ya-XuanZhu Hai-Xia - Lung adenocarcinoma (LUAD) is a prevalent and deadly form of lung cancer. Exercise has been shown to inhibit LUAD progression, yet the underlying molecular mechanisms remain unclear. The transcription factor POU2F2 has been implicated in LUAD tumorigenesis, but its precise role and regulatory targets have not been fully elucidated. - Source: PubMed
Publication date: 2026/03/08
Shi ShujingLeng YumuYang LinfeiZhu BuyiTan HaixinWang FengmingPan JiaqiYang ZhenhuaGu WeiHe Weiwei - The mouse PIWI-interacting RNA (piRNA) pathway provides sustained anti-transposon immunity to the developing male germline by directing transposon DNA methylation. The first step in this process is the recruitment of SPOCD1 to young LINE1 loci. Thereafter, piRNA-mediated tethering of the PIWI protein MIWI2 (also known as PIWIL4) to the nascent transposon transcript recruits the DNA methylation machinery. The piRNA pathway needs to methylate all active transposon copies but how this is achieved remains unknown. Here we show that nuclear piRNA and de novo methylation factors are all euchromatic, exposing constitutive heterochromatin as a genomic blind spot for the piRNA pathway. We discover a 'nowhere-to-hide' mechanism that enables piRNA pathway-mediated LINE1 surveillance of the entire genome. We find that SPOCD1 directly interacts with the nuclear pore component TPR, which forms heterochromatin exclusion zones adjacent to nuclear pores. In fetal gonocytes undergoing piRNA-directed DNA methylation, TPR is found both at the nuclear periphery and throughout the nucleoplasm. We find that the SPOCD1-TPR interaction is required for complete non-stochastic piRNA-directed LINE1 methylation. The loss of the SPOCD1-TPR interaction results in a fraction of SPOCD1 and other chromatin-bound piRNA factors relocalizing to constitutive heterochromatin where they are no longer accessible to MIWI2 and the de novo methylation machinery. In summary, the piRNA pathway has co-opted TPR to guarantee that LINE1s are accessible to the piRNA and de novo methylation machineries. - Source: PubMed
Publication date: 2026/01/14
Chowdhury TamoghnaBoyle ShelaghZoch AnsgarXiang XinyuMirandela Madeleine DiasFieler HannaSpanos ChristosZou JuanKelly DavidBickmore Wendy ACook Atlanta GO'Carroll Dónal - Migraine is a neurovascular disorder that poses a high burden to Veterans, who face a greater risk than sex-matched individuals in the general population. Genetic research on migraine in Veterans and its link to psychiatric comorbidities is limited. We present a meta-analysis of a genome-wide association study (GWAS) of migraine in a predominantly male sample of over 433,000 Veterans, including 87,859 cases, from the Million Veteran Program (MVP), identifying 49 genome-wide significant loci, with 36 novel to this study, of which 7 replicated in an independent prior GWAS (after Bonferroni correction for number of loci tested). Our analyses revealed 283 genes, including some newly associated with migraine: MAML3, CELF4, IRX1, ASXL1, SPOCD1, CXCL, and TLR4. In silico analyses showed enrichment in brain and uterine tissues, which may reflect broader hormonal or neuroendocrine pathways. Compared to previous migraine GWAS, our results show minimal vascular tissue enrichment, potentially reflecting the sample composition, which was predominantly men and Veterans. Migraine SNP-based heritability was 10% for men and 16% for women, and several sex-specific loci were identified through sex-stratified analyses. Despite high genetic correlations with neuropsychiatric disorders - including post-traumatic stress disorder, depression, and traumatic brain injury - Mendelian randomization analyses found no causal links. Finally, we prioritized potential migraine drug targets, including losmapimod (which reduces production of toxic DUX4 protein) and TLR4 antagonists. - Source: PubMed
Publication date: 2025/12/19
Gasperi MariannaRosenthal Sara BrinMaihofer Adam XGerstenberger ArmandDochtermann DanielChoquet HélènePressman AlicePanizzon Matthew SStein Murray BSchuster Nathaniel MPyarajan Saiju Afari NiloofarNievergelt Caroline M - Oral squamous cell carcinoma (OSCC) is one of the most common subtypes of head and neck squamous cell carcinoma (HNSCC), characterized by high recurrence rates and poor prognosis. SPOCD1 has been identified as a facilitator of tumor progression in several cancers; however, its regulatory role in OSCC has not yet been reported. - Source: PubMed
Publication date: 2025/12/09
Hu JianpeiWang ChanyuanWang Lijian