Ask about this productRelated genes to: MRPL44 antibody
- Gene:
- MRPL44 NIH gene
- Name:
- mitochondrial ribosomal protein L44
- Previous symbol:
- -
- Synonyms:
- FLJ12701, FLJ13990
- Chromosome:
- 2q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-12
- Date modifiied:
- 2016-10-05
Related products to: MRPL44 antibody
Related articles to: MRPL44 antibody
- Mitophagy is a critical defense mechanism against metabolic dysfunction-associated steatotic liver disease. MRPL44, a mitochondrial ribosomal protein that regulates mitochondrial DNA-encoded gene expression, has not previously been linked to lipid metabolism. - Source: PubMed
Publication date: 2025/10/02
Liu SiqiXiao LiangguiCheng QiuchenLiao QichaoHuang YuxinLi XianglingZhang ZhiwangXiao YangLuo ZupengPan TingliSun YuSun ChangWang JialeYu LinDamba TurtushikhBatsaikhan BatboldLiang XueLiang YunxiaoBatchuluun KhongorzulLi YixingZhou Lei - B-cell acute lymphoblastic leukemia (B-ALL) is a hematological malignancy characterized by the aberrant accumulation of malignant and immature B cells in the bone marrow. Recent reports including ours have demonstrated that RNA modifications play pivotal roles in B-ALL progression and drug resistance. In the current study, we show that fat mass and obesity-associated protein (FTO), a demethylase of N-methyladenosine (mA) RNA modifications, is highly expressed in relapsed or refractory (R/R) B-ALL patients and B-ALL cell lines. In human B-ALL cells, FTO knockdown inhibited proliferation and cell cycle progression in vitro, while FTO overexpression exhibited opposite effects. Moreover, FTO knockdown significantly attenuated tumorigenesis in vivo after transplantation into immune-compromised mice as shown by reduced tumor burden and extended mouse survival. Interestingly, our research suggested that FTO overexpression resulted in altered cytoplasmic and mitochondrial ribosome biogenesis, and FTO knockdown led to a nucleolar stress-like morphologic change and mitochondrial dysfunction in B-ALL cells. Mechanistically, we found that FTO upregulated the expression of a group of ribosomal proteins via mA-modification, among which RPS15a, RPL9, MRPS16 and MRPL44 were the most prominent ones and confirmed at the mRNA and protein levels. FTO upregulates RPS15a, RPL9, MRPS16 and MRPL44 by mitigating YTHDF2-mediated mA-mRNA decay. Comparatively, although FTO knockdown induced B-ALL cell apoptosis mildly, it synergized with Doxorubicin to promote apparent B-ALL cell death. Furthermore, we found that the FTO inhibitor FB23-2 combined with Doxorubicin markedly repressed B-ALL progression in vivo, accompanied by nucleolar stress-like changes and mitochondrial dysfunction. In summary, our data suggest that FTO is a critical RNA epigenetic promotor of B-ALL, and targeted FTO blockade synergizing with Doxorubicin could be a potential therapy for B-ALL, likely by inhibiting cytoplasmic and mitochondrial ribosome biogenesis. - Source: PubMed
Publication date: 2025/07/05
Li XinxinYang ZiyanHuang SiyongWang JianbinWang XiLiang YingminHan Hua - Hypertrophic cardiomyopathy (HCM) is an autosomal dominant genetic heart disease with a wide range of clinical manifestations, from asymptomatic cases to heart failure and sudden cardiac death. - Source: PubMed
Publication date: 2025/05/22
Gargouri RaniaAmmous-Boukhris NihelHssairi ManelMosbah AmorJabeur MariemFeki WiemMnif ZeinebMokdad-Gargouri RajaAbid LeilaGargouri Lamia - The mitochondrial ribosome (mitoribosome) is responsible for the synthesis of key oxidative phosphorylation subunits encoded by the mitochondrial genome. Defects in mitoribosomal function therefore can have serious consequences for the bioenergetic capacity of the cell. Mutation of the conserved mitoribosomal mL44 protein has been directly linked to childhood cardiomyopathy and progressive neurophysiology issues. To further explore the functional significance of the mL44 protein in supporting mitochondrial protein synthesis, we have performed a mutagenesis study of the yeast mL44 homolog, the MrpL3/mL44 protein. We specifically investigated the conserved hydrophobic pocket region of the MrpL3/mL44 protein, where the known disease-related residue in the human mL44 protein (L156R) is located. While our findings identify a number of residues in this region critical for MrpL3/mL44's ability to support the assembly of translationally active mitoribosomes, the introduction of the disease-related mutation into the equivalent position in the yeast protein (residue A186) was found to not have a major impact on function. The human and yeast mL44 proteins share many similarities in sequence and structure; however results presented here indicate that these two proteins have diverged somewhat in evolution. Finally, we observed that mutation of the MrpL3/mL44 does not impact the translation of all mitochondrial encoded proteins equally, suggesting the mitochondrial translation system may exhibit a transcript hierarchy and prioritization. - Source: PubMed
Publication date: 2024/06/29
Box Jodie MHiggins Margo EStuart Rosemary A - Currently, numerous research endeavors are dedicated to unraveling the intricate nature of neurodegenerative diseases. These conditions are characterized by the gradual and progressive impairment of specific neuronal systems that exhibit anatomical or physiological connections. In particular, in the last twenty years, remarkable efforts have been made to elucidate neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. However, despite extensive research endeavors, no cure or effective treatment has been discovered thus far. With the emergence of studies shedding light on the contribution of mitochondria to the onset and advancement of mitochondrial neurodegenerative disorders, researchers are now directing their investigations toward the development of therapies. These therapies include molecules designed to protect mitochondria and neurons from the detrimental effects of aging, as well as mutant proteins. Our objective is to discuss and evaluate the recent discovery of three mitochondrial ribosomal proteins linked to Alzheimer's and Parkinson's diseases. These proteins represent an intermediate stage in the pathway connecting damaged genes to the two mitochondrial neurological pathologies. This discovery potentially could open new avenues for the production of medicinal substances with curative potential for the treatment of these diseases. - Source: PubMed
Publication date: 2023/07/08
Del Giudice LuigiPontieri PaolaAletta MariarosariaCalcagnile Matteo