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NDUFA13 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. Additionally we are shipping NDUFA13 Proteins (3) and many more products for this protein.
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Human Polyclonal NDUFA13 Primary Antibody for WB - ABIN658141
Sun, Nallar, Raha, Kalakonda, Velalar, Reddy, Kalvakolanu: GRIM-19 and p16(INK4a) synergistically regulate cell cycle progression and E2F1-responsive gene expression. in The Journal of biological chemistry 2010
Show all 3 references for ABIN658141
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
Data suggest that tumor expression of Ki67 (antigen Ki-67 (show MKI67 Antibodies)) and GRIM19 correlate with malignancy in thyroid Hurthle cell (HC) tumors; variable expression of Ki67 (show MKI67 Antibodies) and GRIM19 may helped differentiate HC carcinoma from HC adenoma.
Transfection with eukaryotic plasmid for the simultaneous expression of GRIM19 and LKB1 (show STK11 Antibodies) 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
High expression of GW112 (show OLFM4 Antibodies) in colorectal cancer tissues and reduced expression of GRIM-19 in colorectal cancer tissues may be associated with abnormal proliferation of cancer cells.
Simultaneous expression of ADAM10 (show ADAM10 Antibodies)-specific siRNA and GRIM19 in HepG2 cancer cells significantly inhibited the proliferation, migration and invasion.
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 Antibodies)-induced mortality (GRIM-19) disrupt its anti-signal transducer and activator of transcription 3 (STAT3 (show STAT3 Antibodies)) activity and promote oncogenesis
in vitro nona (show NONO Antibodies)-arginine-GRIM19 treatment of constitutively activated STAT3 (show STAT3 Antibodies) (STAT3c) cancer cells significantly reduced STAT3 (show STAT3 Antibodies)-dependent transcription.
Data show that restoration of GRIM-19 levels reestablishes the control over STAT3 (show STAT3 Antibodies)-dependent gene expression and tumor growth in vivo.
results collectively indicate that viral interferon regulatory factor 1 (show IRF1 Antibodies) modulates interferon (show IFNA Antibodies)/retinoic acid-cell death signals via interactions with GRIM19
GRIM-19 is an inhibitor of signal transducer and activator of transcription 3 (show STAT3 Antibodies)
GRIM-19 suppresses constitutive STAT3 (show STAT3 Antibodies)-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 (show SRC Antibodies)-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