ATMIN
- Known as:
- ATMIN
- Catalog number:
- 002155A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATMIN
Related genes to: ATMIN
- Gene:
- ATMIN NIH gene
- Name:
- ATM interactor
- Previous symbol:
- -
- Synonyms:
- ASCIZ, KIAA0431, ZNF822
- Chromosome:
- 16q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2007-12-06
- Date modifiied:
- 2014-11-19
Related products to: ATMIN
Related articles to: ATMIN
- While the molecular characteristics of cutaneous melanomas (CMs) in individuals with light skin have been extensively studied, less is known about acral melanoma (AM), a non-ultraviolet radiation-induced melanoma more frequently found in individuals with darker skin. Exome and whole genome sequencing of 25 AMs from South African patients with a range of ancestral backgrounds were performed. While close to 50% in CMs, only one AM in a patient of European ancestry harbored an alteration at p.V600 in BRAF. 76% of tumors were triple wild-type. There were hotspot mutations in KIT, mutations in genes encoding components of the MAPK pathway (K57N in MAP2K1 and Y71H in HRAS), and novel candidate driver mutations in genes including PROS1, RGPD3, and SF3A3. Copy number gains included regions with TERT, CDK4, PAK1/GAB2, and DAD1 (chr14q11.2). Gain of chr17q25.1 harboring CDK3 was seen in samples with African ancestry. Eleven significantly deleted regions included chr1q43 (MAP1LC3C) and homozygous deletions of HLA-DRB1, PHF10 (chr6q27), and ATMIN (chr16q23). Mutational signatures included chromosomal instability and chromothripsis. There was a robust ancestry-related difference in tumor evolutionary dynamics where African ancestry was correlated with more genome doubling and clonality with less evolutionary branching. - Source: PubMed
Tod BiancaNam YoonheeKaya Deniz EceKotze MarithaSchneider JohannSanderson-November MichellineVisser Willem IBegani PriyaZhao JunfeiZhu AllenJanuszewski Adamde Wet JohannWedge David CRabadan RaulBowcock Anne M - unlike familial non polyposis colorectal cancer (Lynch syndrome) and familial breast cancer, no genes have been confidently associated with familial lung cancer with the exception of the EGFR and the TP53 genes. Germinal Pathogenetic Variants (GPV) in these two genes account for 0.34-0.9% and 0.8 % lung adenocarcinoma, respectively. - Source: PubMed
Publication date: 2025/04/27
Lintas CPetti RColella GCassano IAzzarà ACortellini ALongo FFrasca LGurrieri FCrucitti P - This study ( = 427) examined the predictive and incremental validity of two Dark Triad (DT) measures-the Dirty Dozen (DD) and the Five-Factor Model Antagonistic Triad Measure (FFM ATM)-in relation to self-reported managerial leadership. Prior research shows that unidimensional DT measures like the DD may obscure nuanced trait-outcome relations. In contrast, the FFM ATM disaggregates DT traits into both core personality components (Antagonism, Emotional Stability, Impulsivity, Agency) and traditional DT subscales (e.g., Psychopathy comprises Antagonism, Emotional Stability, and Impulsivity). Results showed that the FFM ATM provided significantly stronger prediction and incremental validity across leadership dimensions. Both its empirically derived core factors and multidimensional DT subscales explained nearly all variance in leadership outcomes and consistently outperformed the DD in predictive accuracy. These findings highlight the value of capturing the multidimensional structure of DT traits when examining their distinct and overlapping relations with leadership. The results support the use of theoretically grounded, empirically robust instruments like the FFM ATM over brief omnibus measures to provide a more precise understanding of how individual differences in DT traits relate to managerial leaderships. - Source: PubMed
Publication date: 2025/04/08
Phillips Nathaniel LRose LeighaLynam Donald RMiller Joshua D - Oxidative stress-mediated astrocytic damage contributes to nerve injury and the development of depression, especially under stress conditions. Peroxisomes and pexophagy are essential for balancing oxidative stress and protein degradation products. Our previous findings suggest that peroxisome proliferators-activated receptor β/δ (PPARβ/δ) activation significantly alleviates depressive behaviors by preventing astrocytic injury. However, the underlying mechanisms remain unclear. In the present study, we established oxidative injury by treating astrocytes with corticosterone. Subsequently, PPARβ/δ agonists and antagonists were applied to determine the effects of PPARβ/δ on balancing peroxisomes and pexophagy in astrocytes. The PPARβ/δ agonist (GW0742) significantly improved cell viability and decreased intracellular reactive oxygen species (ROS) production induced by corticosterone, while pretreatment with the PPARβ/δ, antagonist GSK3787 reversed the effects of GW0742. Moreover, activating PPARβ/δ promoted peroxisomal biogenesis factor 5 (PEX5)-mediated pexophagy by enhancing the phosphorylation of ataxia-telangiectasia mutated (ATM) kinase. Conversely, blocking PPARβ/δ with GSK3787 partially abolished the effects of GW0742. Further investigations demonstrated that activation of PPARβ/δ not only induced transcription of the ubiquitin protein ligase E3 component n-recognin 5 (UBR5) but also enhanced the interaction between PPARβ/δ and UBR5, contributing to ATM interactor (ATMIN) degradation, and increased phosphorylated ATM kinase levels. Therefore, this study revealed that activating PPARβ/δ improves corticosterone-induced oxidative damage in astrocytes by enhancing pexophagy. PPARβ/δ directly interacts with UBR5 to facilitate ATMIN degradation and promotes ATM phosphorylation, thereby maintaining the balance between peroxisomes and pexophagy. These findings suggest that PPARβ/δ is a potential target for promoting pexophagy in astrocytes upon stress. - Source: PubMed
Ji JuanChen Ye-FanHong ChenRen Xue-WeiXu HangCai Zhen-YuDong Yin-FengSun Xiu-Lan - Li-Fraumeni syndrome (LFS) is a hereditary disorder characterized by an increased risk of developing multiple early-onset cancers, primarily due to germline mutations. Women and men with this mutation face lifetime cancer risks of 90% and 70%, respectively. This report describes the first documented case of LFS with clinical information in Vietnam involving a 9-year-old child diagnosed with osteosarcoma who had multiple first- and second-degree relatives with cancer. Whole-genome sequencing (WGS) revealed a heterozygous, pathogenic, autosomal dominant variant NM_000546.6:c.733G>A (p.Gly245Ser) and a translocation in the 3'UTR of the gene with unknown pathogenicity in both the patient and her mother. Sanger sequencing confirmed the presence of the c.733G>A mutation, which was subsequently detected in extended family members. Of the 17 family members invited for testing, only 8, none of whom currently have cancer, agreed to participate: all tested negative for the mutation. This case highlights the importance of genetic testing for the early detection and management of cancers in LFS patients. It also underscores significant barriers to genetic screening in Vietnam, including limited access and the psychosocial consequences of testing, which emphasize the need for improved genetic counseling and surveillance strategies that are tailored to local contexts. - Source: PubMed
Publication date: 2024/10/08
Le Thanh ThienHa Tung SyTo Linh MaiDang Quang MinhBui Hoa Thi PhuongTran Thanh DucVu Phuong ThiGiang Hoan BaoTran Dung TrungNguyen Xuan-Hung