Ask about this productRelated genes to: MOBKL2B antibody
- Gene:
- MOB3B NIH gene
- Name:
- MOB kinase activator 3B
- Previous symbol:
- MOBKL2B, C9orf35
- Synonyms:
- MOB1D, FLJ13204
- Chromosome:
- 9p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-11
- Date modifiied:
- 2016-10-05
Related products to: MOBKL2B antibody
Related articles to: MOBKL2B antibody
- To map the disease locus for familial ocular melanosis (OM) in the Cairn Terrier. - Source: PubMed
Publication date: 2024/10/24
Winkler Paige ADawson-Baglien Ethan MCoffey Madeline CVenta Patrick JEkenstedt Kari JPetersen-Jones Simon M - Monopolar spindle-binding protein 3B (MOB3B) functions as a signal transducer and altered MOB3B expression is associated with the development of human cancers. - Source: PubMed
Sun JuanZhang Jin-XiuLi Meng-ShiQin Meng-BinCheng Ruo-XiWu Qing-RuChen Qiu-LingYang DanLiao CunLiu Shi-QuanHuang Jie-An - Altered expression and activity of solute carrier family 4 member 4 (SLC4A4) could affect the growth, survival and metastasis of tumor cells. Currently, the role of SLC4A4 in lung adenocarcinoma (LUAD) immunotherapy and prognosis was not entirely clear. - Source: PubMed
Publication date: 2024/07/30
Quan SiyuLi NaLian ShihaiWang YuanyuanLiu YangLiu JianboZhang ZeweiGao DejunLi Yun - Current genome-wide association studies of frontotemporal dementia (FTD) are underpowered due to limited samples. Further, common genetic etiologies between FTD and amyotrophic lateral sclerosis (ALS) remain unknown. Using the largest summary statistics of FTD (3526 cases and 9402 controls) and ALS (27,205 cases and 110,881 controls), we found a significant genetic correlation between them (rˆ = 0.637, P = 0.032) and identified 190 FTD-related variants within 5 loci (3p22.1, 5q35.1, 9p21.2, 19p13.11, and 20q13.13). Among these, ALS and FTD had causal variants in 9p21.2 and 19p13.11. Moreover, MOBP (3p22.1), C9orf72 (9p21.2), MOB3B (9p21.2), UNC13A (19p13.11), SLC9A8 (20q13.13), SNAI1 (20q13.13), and SPATA2 (20q13.13) were discovered by both SNP- and gene-level analyses, which together discovered 15 FTD-associated genes, with 10 not detected before (IFNK, RNF114, SLC9A8, SPATA2, SNAI1, SCFD1, POLDIP2, TMEM97, G2E3, and PIGW). Functional analyses showed these genes were enriched in heart left ventricle, kidney cortex, and some brain regions. Overall, this study provides insights into genetic determinants of FTD and shared genetic etiology underlying FTD and ALS. - Source: PubMed
Publication date: 2023/09/28
Chen KeyingGao TongyuLiu YingZhu KexuanWang TingZeng Ping - We assess the performance of mRNA capture sequencing to identify fusion transcripts in FFPE tissue of different sarcoma types, followed by RT-qPCR confirmation. To validate our workflow, six positive control tumors with a specific chromosomal rearrangement were analyzed using the TruSight RNA Pan-Cancer Panel. Fusion transcript calling by FusionCatcher confirmed these aberrations and enabled the identification of both fusion gene partners and breakpoints. Next, whole-transcriptome TruSeq RNA Exome sequencing was applied to 17 fusion gene-negative alveolar rhabdomyosarcoma (ARMS) or undifferentiated round cell sarcoma (URCS) tumors, for whom fluorescence in situ hybridization (FISH) did not identify the classical pathognomonic rearrangements. For six patients, a pathognomonic fusion transcript was readily detected, i.e., - in two ARMS patients, and -, -, or - in four URCS patients. For the 11 remaining patients, 11 newly identified fusion transcripts were confirmed by RT-qPCR, including -, -, -, -, - and - fusion transcripts in ARMS patients. Additionally, recurrently detected secondary fusion transcripts in patients diagnosed with --positive sarcoma were confirmed (-, -, -, and -). In conclusion, this study shows that mRNA capture sequencing enhances the detection rate of pathognomonic fusions and enables the identification of novel and secondary fusion transcripts in sarcomas. - Source: PubMed
Publication date: 2022/09/20
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