Ask about this productRelated genes to: MPV17L antibody
- Gene:
- MPV17L NIH gene
- Name:
- MPV17 mitochondrial inner membrane protein like
- Previous symbol:
- -
- Synonyms:
- FLJ39599, MLPH1, MLPH2, MPV17L1
- Chromosome:
- 16p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2006-05-12
- Date modifiied:
- 2016-03-15
Related products to: MPV17L antibody
Related articles to: MPV17L antibody
- Acute kidney injury (AKI) is a critical medical condition with limited treatment options and frequently progresses to chronic kidney disease (CKD). This study introduces a novel nanotherapeutic approach based on positively charged cerium-doped polypyrrole nanoparticles [(+)CePPy] for AKI treatment. The positive surface charge of these nanoparticles enhances their cellular uptake and mitochondrial targeting in proximal tubular epithelial cells (PTECs), which play a central role in the pathophysiology of AKI. Comprehensive in vitro and in vivo evaluations demonstrate that (+)CePPy effectively scavenges reactive oxygen species (ROS), ameliorates mitochondrial dysfunction, attenuates apoptosis, and prevents AKI-to-CKD progression. The nanoparticles exhibit excellent biocompatibility and undergo efficient renal clearance within 14 days. Mechanistically, the renoprotective effects involve both direct elimination of ROS and the reinforcement of endogenous antioxidant defenses through upregulation of the Mpv17 mitochondrial membrane protein-like (Mpv17l) pathway. Furthermore, we report that early endosome antigen 1 (EEA1) upregulation mediates the enhanced renal targeting of (+)CePPy under AKI conditions. This research highlights the potential of charge-modulated nanotherapeutics as a translatable strategy for renal protection and presents a promising approach for AKI treatment. - Source: PubMed
Publication date: 2025/12/26
Huang MengjieLiu YuanqiXiao TuoQi PengShen WanjunHuo YingFu BoHao JingAo QiangguoHuo YanhongCai GuangyanChen XiangmeiHong QuanWu MeiyingFeng Zhe - M-LP/Mpv17L (Mpv17-like protein) was initially identified as a novel protein during screening of age-dependently expressed genes in mouse kidney. Previous findings suggested that human Mpv17-like protein (M-LP/MPV17L) is involved in the maintenance of mitochondrial DNA (mtDNA), thus playing a role in cell defense against mitochondrial dysfunction, although its molecular mechanism of action has remained unknown. Recently, generation of M-LP/MPV17L-knockout (KO) cells using CRISPR-Cas9 technology has revealed that M-LP/MPV17L exerts cyclic nucleotide phosphodiesterase (PDE) activity despite lacking the conserved catalytic region and other structural motifs characteristic of the PDE family, and is one of the key components of pathways such as cAMP/cAMP-dependent protein kinase A (PKA) signaling. Moreover, generation of M-LP/Mpv17L-KO mice has revealed that deficiency of M-LP/Mpv17L results in development of β-cell hyperplasia and improved glucose tolerance, as well as physiological afferent cardiac hypertrophy. M-LP/MPV17L is a protein of great interest as it is a potential target for drug development. Therefore, in this review, we overview the molecular characteristics, regulation of expression, cellular functions, phenotypes detected in KO mice, and disease relevance of M-LP/MPV17L. - Source: PubMed
Publication date: 2025/04/01
Iida ReikoYasuda Toshihiro - - Source: PubMed
Publication date: 2024/07/31
Iida ReikoUeki MisuzuYasuda Toshihiro - M-LP/Mpv17L (Mpv17-like protein) is an atypical cyclic nucleotide phosphodiesterase (PDE) without the molecular structure characteristic of the PDE family. Deficiency of M-LP/Mpv17L in mice has been found to result in development of β-cell hyperplasia and improved glucose tolerance. Here, we report another phenotype observed in M-LP/Mpv17L-knockout (KO) mice: afferent cardiac hypertrophy. Although the hearts of M-LP/Mpv17L-KO mice did not differ in size from those of wild-type mice, there was marked narrowing of the left ventricular lumen and thickening of the ventricular wall. The diameter and cross-sectional area of cardiomyocytes in 8-month-old M-LP/Mpv17L-KO mice were increased 1.16-fold and 1.35-fold, respectively, relative to control mice, but showed no obvious abnormalities of cell structure, fibrosis or impaired cardiac function. In 80-day-old KO mice, the expression of hypertrophic marker genes, brain natriuretic peptide (BNF), actin alpha cardiac muscle 1 (ACTC1) and actin alpha 1 skeletal muscle (ACTA1), as well as the Wnt/β-catenin pathway target genes, lymphoid enhancer-binding factor-1 (LEF1), axis inhibition protein 2 (AXIN2) and transcription factor 7 (TCF7), was significantly up-regulated relative to control mice, whereas fibrosis-related genes such as fibronectin 1 (FN1) and connective tissue growth factor (CTGF) were down-regulated. Western blot analysis revealed increased phosphorylation of molecules downstream of the cAMP/PKA signaling pathway, such as β-catenin, ryanodine receptor 2 (RyR2), phospholamban (PLN) and troponin I (cTnI), as well as members of the MEK1-ERK1/2 signaling pathway, which is strongly involved in afferent cardiac hypertrophy. Taken together, these findings indicate that M-LP/Mpv17L is one of the PDEs actively functioning in the heart and that deficiency of M-LP/Mpv17L in mice promotes physiological cardiac hypertrophy. - Source: PubMed
Publication date: 2023/10/18
Iida ReikoUeki MisuzuYasuda Toshihiro - We aimed to characterize the stomach adenocarcinoma (STAD) microbiota and its clinical value using an integrated analysis of the microbiome and transcriptome. Microbiome and transcriptome data were downloaded from the Cancer Microbiome Atlas and the Cancer Genome Atlas databases. We identified nine differentially abundant microbial genera, including , , and , which clustered patients into three subtypes with different survival rates. In total, 74 prognostic genes were screened from 925 feature genes of the subtypes, among which five genes were identified for prognostic model construction, including , , , , and . The prognostic model could stratify patients into different risk groups. The high-risk group was associated with poor overall survival. A nomogram established using the prognostic risk score could accurately predict the 1, 3, and 5 year overall survival probabilities. The high-risk group had a higher proportion of histological grade 3 and recurrence samples. Immune infiltration analysis showed that samples in the high-risk group had a higher abundance of infiltrating neutrophils. The Notch signaling pathway activity showed a significant difference between the high- and low-risk groups. In conclusion, a prognostic model based on five feature genes of microbial subtypes could predict the overall survival for patients with STAD. - Source: PubMed
Publication date: 2023/07/15
Zhou DaxiangXiong ShuXiong JuanDeng XuesongLong QuanzhouLi Yanjie