CNT-Ti Composite 70 Titanium 100 nm
- Known as:
- CNT-Ti Composite 70 Titanium 100 nanometer
- Catalog number:
- T-4031-1
- Product Quantity:
- 1 g
- Category:
- -
- Supplier:
- Bioner
- Gene target:
- CNT- Composite 70 Titanium 100
Ask about this productRelated genes to: CNT-Ti Composite 70 Titanium 100 nm
- Gene:
- ACAP2 NIH gene
- Name:
- ArfGAP with coiled-coil, ankyrin repeat and PH domains 2
- Previous symbol:
- CENTB2
- Synonyms:
- KIAA0041, CNT-B2
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-03
- Date modifiied:
- 2015-08-26
- Gene:
- CCNT1 NIH gene
- Name:
- cyclin T1
- Previous symbol:
- HIVE1
- Synonyms:
- CCNT, CYCT1
- Chromosome:
- 12q13.11-q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-29
- Date modifiied:
- 2018-02-13
- Gene:
- CFDP1 NIH gene
- Name:
- craniofacial development protein 1
- Previous symbol:
- -
- Synonyms:
- BCNT, p97, CP27, SWC5, Yeti, CENP-29
- Chromosome:
- 16q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-09
- Date modifiied:
- 2018-06-14
- Gene:
- CNTD1 NIH gene
- Name:
- cyclin N-terminal domain containing 1
- Previous symbol:
- CNTD
- Synonyms:
- FLJ40137
- Chromosome:
- 17q21.2-q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-12-16
- Date modifiied:
- 2018-02-13
- Gene:
- CNTF NIH gene
- Name:
- ciliary neurotrophic factor
- Previous symbol:
- -
- Synonyms:
- HCNTF
- Chromosome:
- 11q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-07
- Date modifiied:
- 2016-10-05
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- Intrahepatic cholangiocarcinoma (iCCA) is an aggressive malignancy characterized by profound molecular heterogeneity and poor prognosis. Programmed cell death (PCD) regulates tumor progression and shapes the tumor immune microenvironment (TME), yet the roles of distinct PCD subtypes in iCCA remain elusive. Here, we integrated bulk and single-cell transcriptomic datasets derived exclusively from intrahepatic cholangiocarcinoma (iCCA) in TCGA, GEO, and the fan_match cohort, and curated genes representing 21 PCD subtypes. Among 117 machine-learning algorithm combinations, a backward stepwise Cox regression (StepCox) combined with random survival forests (RSF) constructed a robust nine-gene prognostic signature (ATF6, ACVR1, ACAP2, C6orf136, CD4, ABCB9, ABCC1, CSNK2A2, ABCG1) that consistently stratified patients into high- and low-risk groups with distinct outcomes across independent cohorts. High-risk patients exhibited inferior survival, greater immunosuppressive features, elevated TME scores, and enrichment of inflammatory pathways. The PCD score demonstrated predictive value for immunotherapy response across multiple independent cohorts. Single-cell analyses further revealed increased regulatory T-cell infiltration and more complex intercellular communication in high-risk tumors, whereas low-risk tumors displayed stronger collagen signaling and a less immunosuppressive tumor immune microenvironment. Collectively, these findings underscore the importance of PCD-related genes for prognosis and for predicting immunotherapy response in iCCA, and provide a practical framework for risk stratification and therapeutic decision-making. - Source: PubMed
Publication date: 2026/03/16
Zhang TiancaiDou DongqingLiu QiXu DongWang TongLiu RongLu DanyangZhao XiaofangWang SenyanZhang Huapeng - Ovarian cancer (OC) primarily arises from heterogeneous malignant epithelial tissue in the ovary, fallopian tube, or peritoneum. Ubiquitin ligase Ring-finger protein 126 (RNF126) was aberrantly expressed in OC. However, its molecular mechanism is unknown. This study investigates the role and mechanism of RNF126 in regulating ArfGAP with coiled-coil, ankyrin repeat, and PH domains 2 (ACAP2) during OC progression. RT-qPCR and Western blot (WB) were used to assess the expression of RNF126, ACAP2, and lipid synthesis-related genes in OC tissues and cells. The proliferation and migration abilities of OC cells were detected by CCK-8 and Transwell assays. Nile red staining was used to detect the lipid accumulation. The interaction between RNF126 and ACAP2 in OC cells was detected using co-immunoprecipitation (Co-IP). The stability of the ACAP2 protein was analyzed using the cycloheximide (CHX) assay. The effect of RNF126 on tumor growth and metastasis in vivo was investigated by detecting tumor volume and size as well as the number of lung nodules. The expression of RNF126 was upregulated in OC tissues and cells, and RNF126 silencing significantly inhibited the proliferation, migration, and lipid accumulation of OC cells. Mechanistically, ACAP2 was identified as a ubiquitination substrate of RNF126, and its expression was negatively regulated by RNF126. Furthermore, RNF126 promoted OC progression both in vitro and in vivo by suppressing ACAP2 protein expression. RNF126 promotes ovarian cancer progression by reprogramming lipid metabolism via degrading ACAP2. - Source: PubMed
Publication date: 2025/04/18
Wang HaoYan ChaoYe Hong - The study aims to identify potential drug targets for endometrial cancer (EC) subtypes through a Mendelian randomization (MR) approach, assessing their clinical relevance. We utilized genetic instruments for 4,907 plasma proteins from the deCODE Genetics study dataset, and data with EC (n = 12,906) from a genome-wide study (GWAS) meta-analysis in European populations for MR analyses. Complementary analyses included protein-protein interactions (PPI) network analysis, therapeutic efficacy evaluation, differential gene expression assessment, and prognosis evaluation. The expression levels of key drug targets were quantitatively measured at both the transcriptional and translational stages utilizing reverse transcription quantitative PCR (RT-qPCR) and immunohistochemistry (IHC). Additionally, we analyzed various clinicopathological features. Five drug targets for EC (CBR3, GSTO1, HHIP, IGF2R, and MMP10), seven for endometrioid subtypes (ACAP2, CBR3, GSTO1, HHIP, IGF2R, MMP10, and TLR2), and seven for non-endometrioid subtypes (CST3, DNAJB14, FSTL5, GMPR2, IFI16, MAPK9, and NEO1) were identified. Among these, IGF2R (OR = 1.165; 95% CI 1.067-1.272; p = 1.046 × 10) and CST3 (OR = 0.523; 95% CI 0.339-0.804; p = 7.010 × 10) were highlighted as key drug targets with causal evidence both at transcriptional and translational levels. This study preliminarily confirms that IGF2R and CST3 may serve as novel targets for the treatment of EC, providing a foundational reference for innovative clinical approaches to this disease. - Source: PubMed
Publication date: 2024/11/15
Zhu JiameiZhang TingJiang JuanYang MeiXia NanChen Youguo - Ovarian cancer is the most mortality malignancy in gynecology. N7-methylguanosine (m7G) is one of the most prevalent RNA modifications in the development and progression of cancer. The aim of this study is to investigate the effect of m7G-related lncRNA on ovarian cancer in terms of instruction prognosis and immunotherapy. - Source: PubMed
Publication date: 2024/10/08
Li JixinWang HuiZhang SiyangQuan LinruZhou Xin - This study explores the role of disulfidptosis in monocytes and its relation to postmenopausal osteoporosis (PMOP). Using single-cell RNA sequencing and microarray assays, we identified key genes: LONRF1, ACAP2, IPO9, and PGRMC2. Through differential analysis, Weighted Gene Co-expression Network Analysis (WGCNA), and machine learning, these genes were linked to PMOP. Functional enrichment and ROC curve analysis demonstrated their effectiveness in distinguishing postmenopausal fracture patients from healthy individuals. Notably, PGRMC2 exhibited significant expression differences, highlighted by a notable Area Under the Curve (AUC) value of 0.665. Further investigation involved Western blotting and immunohistochemical assays, revealing decreased PGRMC2 expression in ovariectomized (OVX) mice. This decrease was consistent across both experimental methods, emphasizing PGRMC2's role in PMOP. Moreover, PGRMC2 was predominantly present in macrophages compared to monocytes within bone tissue and was significantly located in bone marrow mesenchymal stem cells (BM-MSCs) in PMOP patients. It was also abundantly found in osteoblasts and adipocytes. Additionally, a Mendelian randomization analysis using the TwoSampleMR R package, with data from decode and GWAS databases, was conducted. This analysis showed a significant impact of PGRMC2 on osteoporosis risk (p = 0.0048, OR = 0.6836), suggesting a potential protective effect against the disease. Our results suggest that PGRMC2 may facilitate the differentiation of monocytes into macrophages in bone tissue, influencing the behavior of BM-MSCs. This, in turn, could impact the progression and severity of PMOP. The study provides new insights into the molecular mechanisms underlying postmenopausal osteoporosis and highlights the potential of PGRMC2 as a therapeutic target or biomarker for this condition. - Source: PubMed
Publication date: 2024/08/19
Wang YaobinXiao HefangChen YiSheng XiaoyunFeng ZhiweiPeng BoLiu ZhongchengZhan HongweiXiang DejianZhang ChengjunXia YayiGeng Bin