Recombinant Human 101F6 protein (GST tag N-Terminus)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

The 101F6 protein also known as NADH:cytochrome b5 reductase-like 2 (CYB5RL) functions as a flavoenzyme playing a role in electron transfer processes. It has a molecular weight of approximately 40 kDa. This protein is mainly expressed in the brain and lungs although lower levels can be detected in other tissues. Its localization contributes to its involvement in cellular redox reactions where it assists in maintaining the balance of reduced and oxidized states within cells.

Biological function summary

101F6 acts as a redox partner within electron transfer complexes essential for cellular energy metabolism. It participates actively in redox homeostasis integral in protecting cells against oxidative damage. Though it doesn't form a stable complex itself 101F6 interacts with components of cytochrome systems and impacts the activity of various oxidases and reductases. Its presence indicates a role in maintaining proper redox balance in response to varying cellular conditions.

Pathways

101F6 is involved in two major biological processes: oxidative phosphorylation and electron transport chain pathways. It helps mediate electron transfer to cytochrome c linking it to the broader respiratory chain complex. The protein interacts with cytochrome b5 and other elements of the electron transport chain playing a significant role in cellular respiration and energy production. 101F6 along with these proteins assists in ensuring efficient adenosine triphosphate (ATP) generation.

101F6 has associations with cancer and neurodegenerative diseases. Studies demonstrate altered expression levels of this protein in certain cancer types implicating a potential role in tumor progression. Moreover discrepancies in its redox activity are observed in neurodegenerative disorders such as Alzheimer's disease suggesting its redox function links it to protein targets like amyloid-beta. The connection to these proteins positions 101F6 as an interesting target for therapeutic research aimed at modulating redox states in disease contexts.