OXSR1 Human

OSR1 was first identified as a gene induced under oxidative stress conditions. It has been shown to be essential for the protection of neuronal cells against oxidative stress-induced neurodegeneration . The protein helps control the sensitivity of neuronal cells to oxidative stress, and its overexpression can protect neurons from exogenous stress. Conversely, the absence of OSR1 leads to increased susceptibility to oxidative damage and neurodegeneration .

The protective role of OSR1 is attributed to its ability to regulate the cellular response to oxidative stress. Biochemical assays have indicated that OSR1 itself is susceptible to cysteine-mediated oxidation, which may play a role in its function . Additionally, OSR1 has been shown to be upregulated in both human and pre-symptomatic mouse models of amyotrophic lateral sclerosis (ALS), suggesting its potential as a neuroprotective factor in neurodegenerative diseases .

Research has demonstrated that genetic variants of OSR1 are associated with various health conditions. For instance, certain single nucleotide polymorphisms (SNPs) in the OSR1 gene have been linked to asthma exacerbations in non-smoking asthmatics . This indicates that OSR1 may have broader implications beyond neuroprotection, potentially influencing immune responses and other physiological processes.

Recombinant human OSR1 is used in research to study its role in oxidative stress and related diseases. By understanding how OSR1 functions and its impact on cellular health, scientists aim to develop new therapeutic strategies for conditions associated with oxidative stress. For example, enhancing OSR1 expression or mimicking its activity could be potential approaches to mitigate oxidative damage in neurodegenerative diseases and other disorders.