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CISD1 encodes a protein with a CDGSH iron-sulfur domain and has been shown to bind a redox-active [2Fe-2S] cluster.
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The [2Fe-2S] clusters of mitoNEET are reduced via the formation of a transient complex that brings the [2Fe-2S] clusters of mitoNEET close to the redox-active [2Fe-2S] cluster of anamorsin (show CIAPIN1 Antibodies).
The results suggest that flavin nucleotides may act as electron shuttles to reduce the mitoNEET [2Fe-2S] clusters and regulate mitochondrial functions in human cells.
Data suggest that, compared with oxygen, ubiquinone-2 is more efficient in oxidizing mitoNEET [2Fe-2S] clusters, suggesting that ubiquinone could be an intrinsic electron acceptor of reduced mitoNEET [2Fe-2S] clusters in mitochondrial outer membrane.
CISD1 inhibits ferroptosis by protecting the cells against mitochondrial lipid peroxidation.
the redox-sensing function of mNT is a key component of the cellular adaptive response to help stress-sensitive Fe-S proteins recover from oxidative injury.
A possible role of CISD1 in obesity-associated dysfunctional adipogenesis in human visceral adipose tissue.
Our results confirm the observation that mitoNEET is important in transferring the iron sulfur clusters to the cytosolic aconitase (show ACO1 Antibodies) in living cells and the His-87 ligand in mitoNEET plays important role in this process.
Glutathione reductase (show GSR Antibodies) reduces mitochondrial protein (show COX6B2 Antibodies) mitoNEET [2Fe-2S] clusters.
SNPs in three genes CYP26B1 rs2241057, CISD1 rs2251039, rs2590370, and TBX1 rs4819522 were involved in six potential pathways to influence serum prostate-specific antigen levels.
In this review, we evaluate the current understanding regarding how mitoNEET regulates cellular bioenergetics as well as the structural requirements for drug compound association with mitoNEET
Together, these data suggest that mitoNEET KO mice exhibit many of the characteristics of early neurodegeneration in PD and may provide a novel drug discovery platform to evaluate compounds for enhancing mitochondrial function in neurodegenerative disorders.
mitoNEET protects intact cardiac cells from oxidative stress induced (show SQSTM1 Antibodies) apoptosis during hypoxia and reoxygenation.
The elevation in circulating levels of adiponectin and Fgf15 led to normalized hepatic and serum levels of bile acids, limited hepatic accumulation of toxic bile, attenuated inflammation, and amelioration of liver injury in the ethanol-fed mNT knockout mice.
the mitoNEET-enriched fat pads feature a more vascularized, anti-inflammatory and less fibrotic environment.
The MitoNEET forms a covalent complex with GDH1 (show GLUD1 Antibodies) through disulfide bond formation and acts as an activator.
study found that overexpression of mitoNEET enhances lipid uptake and storage, leading to an expansion of the mass of adipose tissue
mitoNEET is located in mitochondrial fraction of adipocytes.
mitoNEET is located in the mitochondrial fraction of bovine brain.
This gene encodes a protein with a CDGSH iron-sulfur domain and has been shown to bind a redox-active
CDGSH iron sulfur domain-containing protein 1
, zinc finger, CDGSH-type domain 1
, CDGSH iron sulfur domain 1
, CDGSH iron sulfur domain 1 a
, CDGSH iron sulfur domain 1 b
, CDGSH iron-sulfur domain-containing protein 1
, zinc finger CDGSH-type domain 1