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anti-Human NDUFA13 Antibodies:
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Human Polyclonal NDUFA13 Primary Antibody for WB - ABIN537353
Patole, Pawar, Lech, Zecher, Schmidt, Segerer, Ellwart, Henger, Kretzler, Anders: Expression and regulation of Toll-like receptors in lupus-like immune complex glomerulonephritis of MRL-Fas(lpr) mice. in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2006
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Human Polyclonal NDUFA13 Primary Antibody for IF, IHC (p) - ABIN526435
Kjellin, Johansson, Höög, Lehtiö, Jakobsson, Kjellman: Differentially expressed proteins in malignant and benign adrenocortical tumors. in PLoS ONE 2014
These results indicated that rAd-Grim-19 may regulate tumor cell growth and apoptosis. Additionally, the results demonstrated that rAdGrim19 led to beneficial outcomes and prolonged the survival of esophageal tumorbearing mice. In conclusion, the present study demonstrated that rAdGrim19 may have potential as an antitumor agent for esophageal neoplasms
Low GRIM19 expression is associated with radiation resistance in osteosarcoma.
GRIM-19 is a potential predictor of prognosis and disease recurrence in high grade serous carcinoma
Promoting the expression of GRIM19 may yield therapeutic benefits in the treatment of RA.
MiR-6743-5p may act as an oncomiRNA in glioma by targetting GRIM-19 and STAT3.
GRIM-19 suppresses the proliferation and invasion of cutaneous squamous cell carcinoma cells associated with downregulation of STAT3 signaling.
Mitochondrial GRIM-19 could not only serve as an valuable prognostic biomarker for gastric cancer development, but also as a potential therapeutic target for STAT3-dependent carcinogenesis of Gastric cancer.
GRIM-19 expression in cervical cancer cells could inhibit telomerase activity by inhibiting the transactivation of the hTERT promoter by E6, thereby promoting cervical cancer cell senescence.
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) growth and downregulated AKT1 expression, suggesting that GRIM-19 might play a crucial role in hepatocarcinogenesis through negatively regulating the PI3K/AKT signaling pathway.
Low GRIM-19 expression is associated with paclitaxel resistance in cervical cancer.
activation of AMPKalpha 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) and GRIM19 correlate with malignancy in thyroid Hurthle cell (HC) tumors; variable expression of Ki67 and GRIM19 may helped differentiate HC carcinoma from HC adenoma.
Transfection with eukaryotic plasmid for the simultaneous expression of GRIM19 and LKB1 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
Upregulation of GRIM-19 in oral squamous cell carcinoma cells significantly inhibited cell proliferation, migration and invasion in vitro and suppressed tumor growth in vivo.
decreased GRIM-19 expression due to promoter hypermethylation may be important in head and neck carcinogenesis by promoting cell proliferation and regulating metabolic activity
The protein and mRNA levels of GRIM-19 were markedly decreased on Day 4 of pregnancy, but there was no change in GRIM-19 levels in a group of pseudopregnant mice. Overexpression of GRIM-19 decreased the adhesion rate of RL95-2-BeWo co-cultured spheroids and increased apoptosis.
At the basal state, a moderate down-regulation of NDUFA13 created a leak within complex I, resulting in a mild increase in cytoplasm localized Hydrogen Peroxide, but not superoxide. The resultant reactive oxygen species served as a second messenger and was responsible for the STAT3 dimerization and, hence, the activation of antiapoptotic signaling.
iNGR-GRIM-19 has an efficient antitumor activity in vitro and in vivo, and might be a promising agent for the treatment of colorectal cancer.
Transplantation from GRIM19-overexpressing cells downregulated the expression of nuclear factor of activated T cells (NFATc1) but promoted the expression of regulator of calcineurin (RCAN)3 while downregulating NFAT-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-induced mortality (GRIM-19) disrupt its anti-signal transducer and activator of transcription 3 (STAT3) activity and promote oncogenesis
in vitro nona-arginine-GRIM19 treatment of constitutively activated STAT3 (STAT3c) cancer cells significantly reduced STAT3-dependent transcription.
Data show that restoration of GRIM-19 levels reestablishes the control over STAT3-dependent gene expression and tumor growth in vivo.
results collectively indicate that viral interferon regulatory factor 1 modulates interferon/retinoic acid-cell death signals via interactions with GRIM19
GRIM-19 is an inhibitor of signal transducer and activator of transcription 3
GRIM-19 suppresses constitutive STAT3-induced cellular transformation in vitro and in vivo by down-regulating the expression of a number of cellular genes involved in cell proliferation and apoptosis
GRIM-19 inhibits v-Src-induced cell motility by interfering with cytoskeletal restructuring.
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