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NDUFA13 deficiency may be associated with asthenozoospermia through the disturbance of spermatozoa mitochondrial membrane potential and by increasing apoptosis and intracellular reactive oxygen species
GRIM-19 overexpression suppressed hepatocellular carcinoma (HCC (show FAM126A Proteins)) growth and downregulated AKT1 (show AKT1 Proteins) expression, suggesting that GRIM-19 might play a crucial role in hepatocarcinogenesis through negatively regulating the PI3K (show PIK3CA Proteins)/AKT (show AKT1 Proteins) signaling pathway.
Low GRIM-19 expression is associated with paclitaxel resistance in cervical cancer.
activation of AMPKalpha (show GRK4 Proteins) by metformin was associated with a reversal of the suppressed GRIM-19 expression in H9C2 cells, the fold of changes in GRIM-19 expression by metformin were much less in HeLa cells
Data suggest that tumor expression of Ki67 (antigen Ki-67 (show MKI67 Proteins)) and GRIM19 correlate with malignancy in thyroid Hurthle cell (HC) tumors; variable expression of Ki67 (show MKI67 Proteins) and GRIM19 may helped differentiate HC carcinoma from HC adenoma.
Transfection with eukaryotic plasmid for the simultaneous expression of GRIM19 and LKB1 (show STK11 Proteins) more effectively suppressed the growth of breast cancer in vitro and in vivo, and may therefore have therapeutic potential for the treatment of human breast cancer.
Aberrant endometrial expression of GRIM-19 was associated with adenomyosis through the regulation of apoptosis and angiogenesis.
We established here a correlation between the first mutation identified in the NDUFA13 gene, which induces Mitochondrial complex I instability and a severe but slowly evolving clinical presentation affecting the central nervous system.
Upregulation of GRIM-19 also suppressed the secretion of urokinase-type plasminogen activator (u-PA), matrix metalloproteinase (MMP)-2, MMP-9 and vascular endothelial growth factor (VEGF).
GRIM-19 expression is closely associated with colorectal cancer progression and might be a very promising prognostic biomarker
Transplantation from GRIM19-overexpressing cells downregulated the expression of nuclear factor of activated T cells (NFATc1 (show NFATC1 Proteins)) but promoted the expression of regulator of calcineurin (RCAN)3 (show RCAN3 Proteins) while downregulating NFAT (show NFATC1 Proteins)-dependent cytokine gene expression.
GRIM-19 may play important roles in mouse oogenesis and early embryonic development and implantation.
overexpression of GRIM-19 improved the clinical and histologic features of collagen-induced arthritis and also inhibited osteoclast formation.
The deletion of a single copy of the Grim-19 gene was sufficient to promote carcinogenesis and formation of invasive squamous cell carcinomas.
Tumor-derived mutations in the gene associated with retinoid interferon (show IFNA Proteins)-induced mortality (GRIM-19) disrupt its anti-signal transducer and activator of transcription 3 (STAT3 (show STAT3 Proteins)) activity and promote oncogenesis
in vitro nona (show NONO Proteins)-arginine-GRIM19 treatment of constitutively activated STAT3 (show STAT3 Proteins) (STAT3c) cancer cells significantly reduced STAT3 (show STAT3 Proteins)-dependent transcription.
Data show that restoration of GRIM-19 levels reestablishes the control over STAT3 (show STAT3 Proteins)-dependent gene expression and tumor growth in vivo.
results collectively indicate that viral interferon regulatory factor 1 (show IRF1 Proteins) modulates interferon (show IFNA Proteins)/retinoic acid-cell death signals via interactions with GRIM19
GRIM-19 is an inhibitor of signal transducer and activator of transcription 3 (show STAT3 Proteins)
This gene encodes a subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I), which functions in the transfer of electrons from NADH to the respiratory chain. The protein is required for complex I assembly and electron transfer activity. The protein binds the signal transducers and activators of transcription 3 (STAT3) transcription factor, and can function as a tumor suppressor. The human protein purified from mitochondria migrates at approximately 16 kDa. Transcripts originating from an upstream promoter and capable of expressing a protein with a longer N-terminus have been found, but their biological validity has not been determined.
cell death-regulatory protein GRIM19
, NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 13
, GRIM-19 protein
, mitochondrial NADH dehydrogenase ubiquinone 1 alpha subcomplex 13
, NADH dehydrogenase [ubiquinone] 1 alpha subcomplex subunit 13
, OXPHOS complex I B16.6 subunit
, NADH-ubiquinone oxidoreductase B16.6 subunit
, cell death regulatory protein GRIM-19
, complex I B16.6 subunit
, complex I-B16.6
, gene associated with retinoic and IFN-induced mortality 19 protein
, gene associated with retinoic and interferon-induced mortality 19 protein
, gene associated with retinoic-interferon-induced mortality 19 protein
, genes associated with retinoid-IFN-induced mortality 19
, YjeF N-terminal domain containing 3
, mitochondrial complex I subunit Grim19