|Positive WB detected in||A431 cells, human brain tissue|
|Positive IP detected in||A431 cells|
|Positive IHC detected in||human lung cancer tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:500-1:1000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:500-1:1000 for WB|
|Immunohistochemistry (IHC)||IHC : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
11238-1-AP targets NDUFV1 in WB, IP, IHC,ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse, pig, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||NDUFV1 fusion protein Ag1764|
|Full Name||NADH dehydrogenase (ubiquinone) flavoprotein 1, 51kDa|
|Calculated molecular weight||51 kDa|
|Observed molecular weight||51 kDa|
|GenBank accession number||BC015645|
|Gene ID (NCBI)||4723|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
DUFV1(NADH dehydrogenase [ubiquinone] flavoprotein 1, mitochondrial) is also named as UQOR1,Complex I-51kD and belongs to the complex I 51 kDa subunit family. It is the core subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I) that is believed to belong to the minimal assembly required for catalysis. It has 2 isoforms produced by alternative splicing. Defects in NDUFV1 are a cause of Leigh syndrome (LS) and mitochondrial complex I deficiency (MT-C1D).
CLPP deficiency protects against metabolic syndrome but hinders adaptive thermogenesis.
Novel MT-ND Gene Variants Causing Adult-Onset Mitochondrial Disease and Isolated Complex I Deficiency.
Am J Transl Res
Fenofibrate-induced mitochondrial dysfunction and metabolic reprogramming reversal: the anti-tumor effects in gastric carcinoma cells mediated by the PPAR pathway.
Complex I specific increase in superoxide formation and respiration rate by PrP-null mouse brain mitochondria.
Effects of glucose metabolism pathways on nuclear and cytoplasmic maturation of pig oocytes.
J Cell Physiol
Glucose metabolism during in vitro maturation of mouse oocytes: An study using RNA interference.