Adenoviruses are stable at room temperature for short time and are shipped with dry ice . Do not store at -19°C or 5°C for long term. For long term storage, it is recommended to store the viruses at -81°C and avoid repeated freeze-thaw cycles. Before storing at -81°C, it is advisable to make small aliquots to avoid repeated freeze-thaw cycles. Screw cap vials are recommended to decrease chances of the storage buffer desiccating which leads to decrease in infectivity. Diluting the virus is not recommended.
ARHI
- Known as:
- ARHI
- Catalog number:
- 000001A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ARHI
ARHI Adenovirus (Human) an be used directly to transiently over-express your gene of interest in a wide range of host cells. This adenovirus can be used to amplify more adenovirus by transducing HEK293 cells.
Shipping
Adenoviruses are stable at room temperature for short time and are shipped with dry ice . Do not store at -19°C or 5°C for long term. For long term storage, it is recommended to store the viruses at -81°C and avoid repeated freeze-thaw cycles. Before storing at -81°C, it is advisable to make small aliquots to avoid repeated freeze-thaw cycles. Screw cap vials are recommended to decrease chances of the storage buffer desiccating which leads to decrease in infectivity. Diluting the virus is not recommended.
Storage DMEM with 2.5 percent glycerol
Related genes to: ARHI
- Gene:
- DIRAS3 NIH gene
- Name:
- DIRAS family GTPase 3
- Previous symbol:
- ARHI
- Synonyms:
- NOEY2
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-22
- Date modifiied:
- 2019-04-23
Related products to: ARHI
Related articles to: ARHI
- Colorectal cancer (CRC) is a leading cause of cancer death, and the incidence and mortality rates among young adults are rising. Although a subset of CRC cases presents with a family history, suggesting a hereditary component, the specific genetic underpinnings remain incompletely understood, particularly in early-onset CRC (EOCRC). This study aimed to discover novel risk genes for EOCRC using exome sequencing and gene-based rare variant burden testing. Our cohort consisted of 212 European-ancestry cases (174 diagnosed with CRC and 38 with significant polyps) from the South Australian Young Onset Colorectal Polyp and Cancer Study (SAYO) and 31,699 unaffected controls from the Simons Foundation Powering Autism Research for Knowledge (SPARK) cohort. After filtering for ancestry, relatedness, variant quality, and population allele frequency, we performed gene-set and individual-gene burden tests using predicted deleterious missense and loss-of-function variants. Statistical significance was assessed using permutation-corrected binomial testing. An independent validation was conducted in the UK Biobank. Loss-of-function variants in known CRC tumor suppressor genes were significantly enriched in SAYO cases. Gene-level analyses identified as a novel EOCRC susceptibility candidate ( value = 1.0 × 10), with supporting enrichment of deleterious missense and loss-of-function variants in distal colon cancer cases from the UK Biobank. Additional genes (, , , , , and ) demonstrated borderline significance, implicating pathways related to kinetochore assembly, autophagy regulation, and immune signaling. Both predicted gain-of-function and loss-of-function variants contributed to the EOCRC risk, supporting heterogeneous mechanisms of CRC pathogenesis. This study identified novel candidate risk genes for EOCRC, underscoring the role of rare variants and expanding our understanding of the genetic architecture of CRC. Future studies should include functional validation and replication studies on other ancestries to confirm and extend these results. - Source: PubMed
Publication date: 2025/12/09
Song RuocenMikaeel Reger RHe ZhongpingHorsnell MehganUylaki WendyMeng WeiminPoplawski Nicola KWollnik BerndLi YunFeng JinghuaScott Hamish SShen YufengWang ChenYin RuiDing YousongLlor XavierChung Wendy KSmith EricPrice Timothy JYoung Joanne PFan Xiao - Mutations in KRAS drive 88% of pancreatic ductal adenocarcinomas (PDAC) and up to 40% of low-grade serous ovarian cancers (LGSOC), making KRAS a long-standing therapeutic target. We previously showed that DIRAS3 binds RAS, forming heterodimers that disrupt RAS clustering and downstream MAPK signaling. Building on this, we developed conformationally constrained DIRAS3-derived peptides using two cyclization strategies and characterized them by NMR and biolayer interferometry. These cyclic peptides attenuate the interaction between KRAS and the BRAF RAS-binding domain, penetrate cells efficiently, and inhibit KRAS nanoclustering on the inner leaflet of the plasma membrane. Functionally, they reduce cell viability and suppress PDAC and LGSOC growth in cell culture and xenograft models. Our findings demonstrate that DIRAS3-based cyclic peptides represent a distinct strategy to directly inhibit oncogenic KRAS signaling and provide a promising framework for therapeutic development in KRAS-driven cancers. - Source: PubMed
Publication date: 2025/10/04
Gray Joshua PBildik GamzeKim Ha-NeulSutton Margie NWang JingOsuji Amarachi OBatistatou NefeliYang HailingMao WeiqunTan ZhiGasmi-Seabrook Geneviève M CLiu JunchenHancock John FMarshall Christopher BKritzer Joshua AIkura MitsuhikoBast Robert CMillward Steven WLu Zhen - Cardioembolic stroke is a major complication of atrial fibrillation (AF). We investigated differentially expressed genes (DEGs) in the left atrial appendage (LAA) with and without LAA thrombus (LAAT) using RNA sequencing (RNA-seq). LAA tissue samples were obtained during cardiac surgery. We analyzed samples with LAAT (n = 6) and without LAAT (n = 5). Differential gene expression analysis was conducted to identify significantly altered genes. RNA-seq identified 27 differentially expressed genes (false discovery rate < 0.05,|log(fold change)| >2). Among these, four DEGs-DIRAS3, CYP26B1, PRG4, and ITLN1-exhibited particularly large fold changes. Protein-protein interaction network analysis revealed two hub genes, FKBP5 and TUBA3D, based on degree (≥ 30) and betweenness centrality (≥ 3000). Quantitative PCR confirmed consistent expression patterns for these genes. Furthermore, consistent results were obtained in another independent set (10 cases with LAAT and 10 cases without LAAT). Linear regression analysis, adjusted for age and gender, showed that DIRAS3 expression was significantly associated with both the fibrosis ratio (β = 2.99, 95% confidence interval [CI] 0.22-5.75, p = 0.034) and NT-proBNP levels (β = 373, 95% CI 238-507, p= 5.71E-08). Additionally, CYP26B1 and TUBA3D expression levels were significantly associated with NT-proBNP (β = 349, 95% CI 23.8-674, p= 0.036; β = -140, 95% CI -272 to -8.81, p = 0.038, respectively). We identified candidate genes potentially involved in LAAT in AF patients through RNA-seq analysis. These findings may elucidate the molecular mechanisms underlying LAAT pathogenesis. - Source: PubMed
Publication date: 2025/10/05
Maeda JunjiFurutani MotokiMiyauchi ShunsukeNakashima MikaIshibashi NaokiSakai TakumiOguri NaotoMiyamoto ShogoOkamura ShoOkubo YousakuTokuyama TakehitoOda NoboruTakasaki TaiichiTakahashi ShinyaAizawa HidenoriShigemizu DaichiNakano Yukiko - Prognoses for patients with clear cell renal cell carcinoma (ccRCC) are associated with complex interactions between tumor and patient characteristics. This study investigated associations between body composition and tumor proteomics and their interaction with survival among patients with ccRCC. - Source: PubMed
Publication date: 2025/09/21
Mahenge Cuthbert MarioAkasheh Rand TalalNguyen XuanCheng Ting-Yuan David - Autophagy is a crucial cellular process responsible for sustaining homeostasis through the degradation and recycling of proteins and organelles, providing energy during amino acid starvation and hypoxia. In cancer, autophagy can either inhibit tumor growth or support cancer cell survival. Our previous studies have shown that re-expression of the tumor suppressor gene inhibits growth of ovarian cancer cells, promotes autophagic cell death in vitro, and induces tumor dormancy in vivo. Growth factors and extracellular matrix (ECM) components can, however, inhibit DIRAS3-induced autophagic cell death. This study explores whether fibronectin (FN) can counteract the growth inhibition induced by DIRAS3 in ovarian cancer cells. FN was found to inhibit DIRAS3-induced autophagy and to partially rescue ovarian cancer cells from DIRAS3-induced cell death while reducing DIRAS3-induced inhibition of p-FAK and p-AKT. Inhibiting FAK with defactinib in ovarian cancer cells enhanced DIRAS3-induced autophagy and cell death. Re-expression of DIRAS3 and treatment with defactinib produced tumor regression in xenograft models. Our findings suggest that ECM components in the tumor microenvironment like FN enhance the activities of β1 integrin, FAK, and AKT to inhibit DIRAS3-induced autophagic cell death, thereby promoting ovarian cancer cell survival. - Source: PubMed
Publication date: 2025/08/13
Guo JingSantiago-O'Farrill Janice MOrellana VivianOzyurt RumeysaYang HailingPina MarcBildik GamzeMao WeiqunBast Robert CLu Zhen