Tap2 siRNA_Lentivectors
- Known as:
- Tap2 siRNA_Lentivectors
- Catalog number:
- i065468c
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Tap2 siRNA_Lentivectors
Related genes to: Tap2 siRNA_Lentivectors
- Gene:
- TAP2 NIH gene
- Name:
- transporter 2, ATP binding cassette subfamily B member
- Previous symbol:
- ABCB3
- Synonyms:
- PSF2, RING11, D6S217E
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-25
- Date modifiied:
- 2019-04-23
Related products to: Tap2 siRNA_Lentivectors
Related articles to: Tap2 siRNA_Lentivectors
- Why only a minority of hyperuricaemic individuals develop gout remains unclear, and epigenetic differences between these states are poorly characterised. We aimed to define DNA methylation signatures distinguishing gout from asymptomatic hyperuricaemia and evaluate their utility for molecular stratification. - Source: PubMed
Publication date: 2026/09/29
Chen ZiyiRen HaofanJi XiaopengDong BingziJi Aichang - Head and neck squamous cell carcinoma (HNSCC) exhibits heterogeneous responses to radiotherapy; however, the underlying multi-omics regulatory networks remain poorly characterized. This study elucidated the distinct post-translational modification (PTM) landscapes induced by X-ray and carbon-ion irradiation. - Source: PubMed
Publication date: 2026/09/27
Xia Fan-TongLiao Zhi-YunCai Si-QiZhou Li-RongYang Meng-QiZhang XinLi DanZhang HuanLiu Yun-ChangYang Jie-YingJiang JiaHu Yi-HongSui Jiang-DongWang Ying - Antenatal depressive symptoms (ADS) are common during pregnancy and are linked to adverse maternal and offspring neurodevelopmental outcomes. The placenta plays a central role in maternal-fetal communication and may function as an epigenetic sensor of maternal psychological stress. However, placental epigenetic signatures associated with ADS remain poorly understood. This study investigated epigenome-wide placental DNA methylation patterns associated with ADS in an Indian cohort. Placental samples were collected at delivery from women recruited in early pregnancy into the STRiDE cohort. Depressive symptoms were assessed at 24-28 weeks' gestation using the Patient Health Questionnaire-9 (PHQ-9). Participants were classified as controls (PHQ-9 ≤ 4; n = 53) or ADS (PHQ-9 > 4; n = 54). Genome-wide DNA methylation profiling was performed using the Illumina Infinium MethylationEPIC array. Epigenome-wide association analysis identified no CpG sites that remained statistically significant after Benjamini-Hochberg FDR correction. Top nominal CpGs showed medium-to-large effect sizes for ADS. Exploratory analyses of the top nominally associated CpGs annotated to genes including TAP2, LRCH1, SLITRK2, RASSF1 and IL3 implicated in immune regulation, cellular signalling and neurodevelopment. Gene enrichment analysis suggested the involvement of biological processes and pathways related to synaptic organization, ion transport, Hippo signalling, and thyroid hormone regulation. In conclusion, the study findings provide preliminary evidence of DNA methylation signatures linked to potential candidate genes and biological pathways that may be relevant to ADS, supporting the need for validation in larger independent cohorts and functional experimental studies. - Source: PubMed
Publication date: 2026/09/15
Thirumoorthy ChinnasamyDarveekaran Nair Sree SankarDeepa MohanRam UmaAnjana Ranjit MohanBalasubramanyam MuthuswamyMohan ViswanathanSaravanan PonnusamyGokulakrishnan Kuppan - Cancer progression is sustained by complex interactions between oncogenic signaling pathways and immune checkpoint networks, yet their mechanistic crosstalk remains poorly integrated in existing reviews. This review synthesises the bidirectional regulatory relationships between oncogenic signaling and immune checkpoints, with emphasis on mechanistic interdependencies, therapeutic resistance, and precision oncology strategies. - Source: PubMed
Publication date: 2026/08/18
Sekar Praveen Kumar ChandraVeerabathiran Ramakrishnan - Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide. Approximately 15% of localized and 5% of metastatic cases exhibit mismatch repair deficiency (dMMR) or high microsatellite instability (MSI-H). While immune checkpoint inhibitors (ICIs) have revolutionized the first-line treatment for this subgroup, 15%-46% of patients experience primary resistance, and a subset of responders eventually acquires resistance. This review synthesizes the multifaceted mechanisms underlying ICI resistance in dMMR/MSI-H CRC. We delineate tumor-intrinsic alterations, including defects in the antigen presentation machinery (specifically transporter associated with antigen processing [TAP]1/TAP2 and β-microglobulin [βm]), oncogenic signaling via the Wnt/β-catenin and JAK/STAT pathways, and epigenetic remodeling involving ARID1A. Furthermore, we explore the role of the immunosuppressive tumor microenvironment (TME), characterized by T-cell exclusion and myeloid-derived suppressor cell (MDSC) accumulation. To address these barriers, we evaluate the clinical potential of third-generation ICIs targeting lymphocyte activation gene 3 (LAG-3), T-cell immunoglobulin and mucin-domain-containing-3 (TIM-3), and TIGIT, as well as emerging biomarker strategies such as gut microbiome modulation and circulating tumor DNA (ctDNA) dynamics. By integrating these mechanistic insights with novel therapeutic approaches, including bispecific antibodies (BsAbs) and adoptive cell transfer, this review aims to provide a roadmap for overcoming resistance and advancing precision immunotherapy in dMMR/MSI-H CRC. - Source: PubMed
Zhou KeLu PingXu HongliLiang Xinjun