MT-ND6 Antibodies

NADH-ubiquinone oxidoreductase chain 6 (MT-ND6)

Core subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I) that is believed to belong to the minimal assembly required for catalysis. Complex I functions in the transfer of electrons from NADH to the respiratory chain.

The immediate electron acceptor for the enzyme is believed to be ubiquinone (By similarity). .

Gene Information

Human
Gene Name:	MT-ND6
Uniprot:	P03923
Entrez:

Family

Belongs to:
complex I subunit 6 family

Alternative Names

NADH-ubiquinone oxidoreductase chain 6

Molecular Weight

Mass (kDA):
18.622 kDA

Genomic Context

Human
Location:
Sequence:	;

Subcellular Localizations

Mitochondrion membrane; Multi-pass membrane protein.

Diseases

• Leber hereditary optic neuropathy (LHON)

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/MT-ND6

Best Uses Of The MT-ND6 Marker

If you're looking to find a new antibody for your research, you might be curious what it is all about. You've probably heard about the MT-ND6 marker, but did you know that this gene and protein actually do something? You're not the only one. This article will give you all the details. Ultimately, this article will explain what the MT-ND6 marker is and how you can use it in your own research.

MT-ND6 Signer

The MT–ND6 gene is a component of the complex 1 enzyme complex. It functions inside mitochondria, which are cellular structures responsible for converting food into energy. The MT ND6 enzyme participates in oxidative phosphorylation. This involves the use of simple sugars, oxygen, and ATP to create adenosinetriphosphate. ATP is the cell's main energy source.

MT-ND6 protein

The secondary structure MT-ND6 was predicted using homology based modeling and computational chemistry. Six hydrophobic domains were predicted and five loops. The protein is similar to normal proteins, with the predicted loops and hydrophobic domains aligning with its hydropathy plot. A normal protein was also shown as a reference. The mutations of the MT-ND6 protein included M14V mutation in M010b cells, M64V mutation in LHON and A72V in LHON.

Cellular respiration is mediated by ND6 proteins. This process depends on proton flux. This protein is susceptible to mutations that can cause vision loss in one or both of the eyes. There is no recovery. Antigens for the MTND6 proteins may be beneficial in this instance. They could also prevent the development or progression of other disease-causing disorders. MT-ND6 protein is a promising treatment option for ND6-related ocular diseases.

The MT–ND6 MT protein is made from the MT–ND6 Gene. This protein is part of the complex I enzyme complex. It is active in the mitochondria. It uses oxygen and simple sugars to produce ATP, a source of energy for the cell. Although ATP can be converted to energy in the body, it requires a lot of food. The mitochondria of cells actually generate the energy required by the cells.

The MT–ND6 genetic code is located on the L strand the human mitochondrial genomic genome. It is one seven genes that code the NADH deshydrogenase. Boster Bio's MTND6 product is also available as a recombinant. While the MT-ND6 protein is only one of the many products of this type, the protein's mtDNA copy number is significant.

This mutation causes a subtle defect in Complex I of M010b cells. In contrast to the 14488 ND6 mutation seen in the LHON patient, the T14634C mutation in M010b cells is closer to that of mutagenized rodent cells. These two mutations are associated with the MT-ND6 phenotype seen in LHON. The data presented in the article have several limitations.

MT-ND6 gene

The MT–ND6 protein encodes a protein named NADH Dehydrogenase 6. This enzyme is a part of the complex-I enzyme complex. These enzymes play a crucial role in mitochondria. They are cellular structures which convert food into fuel. These enzymes are responsible for oxidative phosphorylation which uses oxygen and simple glucose to produce adenosinetriphosphate. ATP is the cell’s primary source for energy.

Increased expression of TFAM reduced steady-state MT-ND6 transcript levels in human osteosarcoma cells. It did not alter the copy count of mtDNA. These results were similar to those seen in transgenic mice. The mRNA expression levels for MTCO1 & MTND6 were also higher, indicating that mtDNA was induced.