Ask about this productRelated genes to: GTPBP10 Blocking Peptide
- Gene:
- GTPBP10 NIH gene
- Name:
- GTP binding protein 10
- Previous symbol:
- -
- Synonyms:
- DKFZP686A10121, FLJ38242, OBGH2
- Chromosome:
- 7q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-15
- Date modifiied:
- 2016-05-04
Related products to: GTPBP10 Blocking Peptide
Related articles to: GTPBP10 Blocking Peptide
- Mitochondria contain their own genetic information and a dedicated translation system to express it. The mitochondrial ribosome is assembled from mitochondrial-encoded RNA and nuclear-encoded ribosomal proteins. Assembly is coordinated in the mitochondrial matrix by biogenesis factors that transiently associate with the maturing particle. Here, we present a structural snapshot of a large mitoribosomal subunit assembly intermediate containing 7 biogenesis factors including the GTPases GTPBP7 and GTPBP10. Our structure illustrates how GTPBP10 aids the folding of the ribosomal RNA during the biogenesis process, how this process is related to bacterial ribosome biogenesis, and why mitochondria require two biogenesis factors in contrast to only one in bacteria. - Source: PubMed
Publication date: 2023/12/02
Nguyen Thu GiangRitter ChristinaKummer Eva - As a heterogeneous group of hematologic malignancies, leukemia has been widely studied at the transcriptome level. However, a comprehensive transcriptomic landscape and resources for different leukemia subtypes are lacking. Thus, in this study, we integrated the RNA sequencing data sets of >3000 samples from 14 leukemia subtypes and 53 related cell lines via a unified analysis pipeline. We depicted the corresponding transcriptomic landscape and developed a user-friendly data portal LeukemiaDB. LeukemiaDB was designed with 5 main modules: protein-coding gene, long noncoding RNA (lncRNA), circular RNA, alternative splicing, and fusion gene modules. In LeukemiaDB, users can search and browse the expression level, regulatory modules, and molecular information across leukemia subtypes or cell lines. In addition, a comprehensive analysis of data in LeukemiaDB demonstrates that (1) different leukemia subtypes or cell lines have similar expression distribution of the protein-coding gene and lncRNA; (2) some alternative splicing events are shared among nearly all leukemia subtypes, for example, MYL6 in A3SS, MYB in A5SS, HMBS in retained intron, GTPBP10 in mutually exclusive exons, and POLL in skipped exon; (3) some leukemia-specific protein-coding genes, for example, ABCA6, ARHGAP44, WNT3, and BLACE, and fusion genes, for example, BCR-ABL1 and KMT2A-AFF1 are involved in leukemogenesis; (4) some highly correlated regulatory modules were also identified in different leukemia subtypes, for example, the HOXA9 module in acute myeloid leukemia and the NOTCH1 module in T-cell acute lymphoblastic leukemia. In summary, the developed LeukemiaDB provides valuable insights into oncogenesis and progression of leukemia and, to the best of our knowledge, is the most comprehensive transcriptome resource of human leukemia available to the research community. - Source: PubMed
Luo MeiMiao Ya-RuKe Ya-JuanGuo An-YuanZhang Qiong - At present, cancer is still one of the principal diseases to represent a serious danger to human health. Although research on the pathogenesis and treatment of cancer is progressing rapidly, the current knowledge on this topic is far from sufficient. Some tumors with poor prognoses lack effective prognostic biomarkers. - Source: PubMed
Publication date: 2022/03/23
Hu YimingChen LiangTang QikaiWei WeiCao YuanXie JiahengJi Jing - Huntington's disease (HD) is a neurodegenerative disease. MicroRNAs (miRNAs) are small non-coding RNAs that mediate post-transcriptional regulation of target genes. Although miRNAs are extensively edited in human brains, the editome of miRNAs in brains of HD patients is largely unknown. By analyzing the small RNA sequencing profiles of brain tissues of 28 HD patients and 83 normal controls, 1182 miRNA editing sites with significant editing levels were identified. In addition to 27 A-to-I editing sites, we identified 3 conserved C-to-U editing sites in miRNAs of HD patients. 30 SNPs in the miRNAs of HD patients were also identified. Furthermore, 129 miRNA editing events demonstrated significantly different editing levels in prefrontal cortex samples of HD patients (HD-PC) when compared to those of healthy controls. We found that hsa-mir-10b-5p was edited to have an additional cytosine at 5'-end in HD-PC, and the edited hsa-mir-10b repressed GTPBP10 that was often downregulated in HD. The down-regulation of GTPBP10 might contribute to the progression of HD by causing gradual loss of function of mitochondrial. These results provide the first endeavor to characterize the miRNA editing events in HD and their potential functions. - Source: PubMed
Publication date: 2022/02/24
Guo ShiyongYang JunJiang BingbingZhou NanDing HaoZhou GuangchenWu ShuaiSuo AngbajiWu XingwangXie WenpingLi WanranLiu YulongDeng WeiZheng Yun - Assembly of the mitoribosome is largely enigmatic and involves numerous assembly factors. Little is known about their function and the architectural transitions of the pre-ribosomal intermediates. Here, we solve cryo-EM structures of the human 39S large subunit pre-ribosomes, representing five distinct late states. Besides the MALSU1 complex used as bait for affinity purification, we identify several assembly factors, including the DDX28 helicase, MRM3, GTPBP10 and the NSUN4-mTERF4 complex, all of which keep the 16S rRNA in immature conformations. The late transitions mainly involve rRNA domains IV and V, which form the central protuberance, the intersubunit side and the peptidyltransferase center of the 39S subunit. Unexpectedly, we find deacylated tRNA in the ribosomal E-site, suggesting a role in 39S assembly. Taken together, our study provides an architectural inventory of the distinct late assembly phase of the human 39S mitoribosome. - Source: PubMed
Publication date: 2021/07/27
Cheng JingdongBerninghausen OttoBeckmann Roland