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anti-Human NDUFA13 Antikörper:
anti-Mouse (Murine) NDUFA13 Antikörper:
anti-Rat (Rattus) NDUFA13 Antikörper:
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Human Polyclonal NDUFA13 Primary Antibody für 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 für IF, IHC (p) - ABIN526435
Kjellin, Johansson, Höög, Lehtiö, Jakobsson, Kjellman: Differentially expressed proteins in malignant and benign adrenocortical tumors. in PLoS ONE 2014
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 (zeige STAT3 Antikörper)-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 (zeige FAM126A Antikörper)) growth and downregulated AKT1 (zeige AKT1 Antikörper) expression, suggesting that GRIM-19 might play a crucial role in hepatocarcinogenesis through negatively regulating the PI3K (zeige PIK3CA Antikörper)/AKT (zeige AKT1 Antikörper) signaling pathway.
Low GRIM-19 expression is associated with paclitaxel resistance in cervical cancer.
activation of AMPKalpha (zeige GRK4 Antikörper) 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 (zeige MKI67 Antikörper)) and GRIM19 correlate with malignancy in thyroid Hurthle cell (HC) tumors; variable expression of Ki67 (zeige MKI67 Antikörper) and GRIM19 may helped differentiate HC carcinoma from HC adenoma.
Transfection with eukaryotic plasmid for the simultaneous expression of GRIM19 and LKB1 (zeige STK11 Antikörper) 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.
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 (zeige NFATC1 Antikörper)) but promoted the expression of regulator of calcineurin (RCAN)3 (zeige RCAN3 Antikörper) while downregulating NFAT (zeige NFATC1 Antikörper)-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 (zeige IFNA Antikörper)-induced mortality (GRIM-19) disrupt its anti-signal transducer and activator of transcription 3 (STAT3 (zeige STAT3 Antikörper)) activity and promote oncogenesis
in vitro nona (zeige NONO Antikörper)-arginine-GRIM19 treatment of constitutively activated STAT3 (zeige STAT3 Antikörper) (STAT3c) cancer cells significantly reduced STAT3 (zeige STAT3 Antikörper)-dependent transcription.
Data show that restoration of GRIM-19 levels reestablishes the control over STAT3 (zeige STAT3 Antikörper)-dependent gene expression and tumor growth in vivo.
results collectively indicate that viral interferon regulatory factor 1 (zeige IRF1 Antikörper) modulates interferon (zeige IFNA Antikörper)/retinoic acid-cell death signals via interactions with GRIM19
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