LRPPRC (Leucine Rich Pentatricopeptide Repeat Containing)

These analyses identify atrophy-associated PTMs that provide refined biomarkers for fingerprinting the atrophic stimulus. Although most PTMs are stimulus-specific, P27 dihydroxylation of Lrpprc declines during muscle wasting induced by cancer, dexamethasone and aging, suggesting that this is a general atrophy marker. Experimental up-regulation of the atrophy-mimicking variant LrpprcP27A reduces muscle force compared to wild-type Lrpprc in young and old mice, suggesting that atrophy-associated P27 dihydroxylation contributes to disease-associated muscle weakness.

Our study uncovers a "C1orf35-driven" energy metabolism model in MM cells, providing new insights into the pathogenesis of MM and a potential novel target for the treatment of cancer cells with a high"C1orf35-driven" anabolic metabolism. Schematic diagram of C1orf35 simultaneously promotes glycolysis and OXPHOS.

Importantly, PRKAB2 overexpression significantly restored sensitivity to tyrosine kinase inhibitors (TKIs) in sunitinib-resistant RCC cells...Overall, our findings identify PRKAB2 as a critical tumor suppressor in RCC, regulating both protein-protein interactions and lipid metabolism to suppress mitophagy. Targeting PRKAB2-associated pathways may provide a promising therapeutic strategy to enhance treatment efficacy and overcome drug resistance in RCC.

Our findings suggest that LRPPRC may serve as a promising biomarker for HNSCC prognosis and a therapeutic target for controlling cancer metastases and enhancing patient outcomes, while being a predictor for immune therapy response as well.

Moreover, FKA-9i exhibits a synergistic enhancement effect when combined with chemotherapeutic drugs, YBX1 and RPN1 inhibitors, as well as drugs targeting the glycolysis pathway. This study firmly establishes FKA-9i as an anti-tumor leading compound by targeting the LRPPRC-YBX1-RPN1 mediated MAPK regulatory network, offering a novel strategy to surmount the clinical translation hurdles of natural flavonoids.

This inhibition collectively diminishes the expression and activity changes in complex IV, induces mitochondrial dysfunction, and promotes cuproptosis in ovarian cancer. This study further demonstrates that inhibiting the oxidative phosphorylation complex IV can enhance copper-induced cell death in ovarian cancer.

Current LRPPRC inhibitors often suffer from suboptimal specificity and binding affinity. Advancing clinical translation requires co-crystal structures of LRPPRC for rational drug design and novel delivery strategies to enhance mitochondrial enrichment of inhibitors.

Clinically, UCBs exhibiting high circRCP and LRPPRC expression had the worst outcomes. Taken together, we have identified a mitochondria-located circRNA that protects UCB cells from oxidative stress, highlighting its potential role in UCB pathogenesis and warranting further investigation into its therapeutic applicability.

The 4 MRGs may contribute to the understanding on UPRmt in LUAD and the development of relevant medicine in clinical practice.

Furthermore, ubiquitous simultaneous overexpression of Polrmt and Lrpprc, which stabilizes mitochondrial messenger RNAs, did not increase steady-state levels of mitochondrial transcripts in the mouse. Our data show that POLRMT levels regulate transcription initiation, but additional regulatory steps downstream of transcription initiation and transcript stability limit OXPHOS biogenesis.

Our study identifies OXSM as a key DRG hub gene in glioma, with elevated expression strongly correlating with poor patient prognosis. The observed relationship between OXSM expression and immune cell infiltration suggests its potential role in modulating the glioma microenvironment. These findings advance our understanding of glioma's molecular mechanisms and may inform the development of novel therapeutic strategies.

Gene expression analysis further supported these findings, showing significant upregulation of LRPPRC (P < 0.001) and downregulation of ABCG5 (P < 0.001) in BTC tissues, confirming their roles in carcinogenesis. This study provides compelling evidence for a genetic association between cholelithiasis and BTC, highlighting the role of genetic variants in ABCG5/8 and LRPPRC in mediating these conditions.