Peroxiredoxin-1 Antibodies

Peroxiredoxin-1 (PRDX1)

Thiol-specific peroxidase which catalyzes the reduction of hydrogen peroxide and organic hydroperoxides to water and alcohols, respectively. Plays a role in cell protection against oxidative stress by detoxifying peroxides and as sensor of hydrogen peroxide-mediated signaling events.

Might take part in the signaling cascades of growth factors and tumor necrosis factor-alpha by regulating the intracellular concentrations of H(2)O(2) (PubMed:9497357). Reduces an intramolecular disulfide bond in GDPD5 that gates the capability to GDPD5 to induce postmitotic motor neuron differentiation (By similarity).

Gene Information

Human
Gene Name:	PRDX1
Uniprot:	Q06830
Entrez:	5052

Family

Belongs to:
peroxiredoxin family

Alternative Names

EC 1.11.1; EC 1.11.1.15; Natural killer cell-enhancing factor A; natural killer-enhancing factor A; NKEFA; NKEF-A; PAG; PAGAMSP23; PAGB; Peroxiredoxin 1; peroxiredoxin-1; PRDX1; proliferation-associated gene A; Proliferation-associated gene protein; PRX1; PRXI; TDPX2; Thioredoxin peroxidase 2; Thioredoxin-dependent peroxide reductase 2

Molecular Weight

Mass (kDA):
22.11 kDA

Genomic Context

Human
Location:	1p34.1
Sequence:	1; NC_000001.11 (45511035..45522890, complement)

Subcellular Localizations

Cytoplasm. Melanosome. Identified by mass spectrometry in melanosome fractions from stage I to stage IV.

Diseases

• Malignant Neoplasms
• Neoplasms
• Carcinoma
• Lung Neoplasms
• Adenocarcinoma
• Carcinogenesis
• Cell Transformation, Neoplastic
• Malignant Neoplasm Of Lung
• Inflammation
• Diabetes Mellitus
• Malignant Paraganglionic Neoplasm
• Malignant Squamous Cell Neoplasm
• Neoplasm Metastasis

• Malignant Neoplasm Of Breast
• Neurodegenerative Disorders
• Esophageal Neoplasms
• Tumor Progression
• Alzheimer's Disease
• Diabetes Mellitus, Non-insulin-dependent
• Liver Neoplasms

Interacting Proteins

• AR
• PRNP
• PTEN
• SRXN1
• STK4

• TERF1
• TPT1

Pathways

• Cell Death
• Cell Proliferation
• Pathogenesis
• Response To Oxidative Stress
• Localization
• Cell Differentiation
• Cell Cycle
• Translation
• Neuroprotection
• Cell Migration
• Embryo Development
• Oocyte Maturation
• Transport

• Aging
• Oxidative Phosphorylation
• Flight
• Protein Oxidation
• Cell Growth
• Rna Interference
• Dna Repair

PTMs

• Oxidation
• Phosphorylation
• Reduction
• Acetylation

• Methylation
• Ubiquitination
• Glutathionylation
• Glycosylation

• Deglutathionylation

Research Areas

• Core ESC-Like Genes
• Stem Cell Markers

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/PRDX1

Boster Bio - Best Uses Of The PRDX1 Marker

PRDX1 is a highly important protein that regulates various physiological processes, such as lipophagic flux and regulation of tubular senescence. Boster Bio scientists can submit their results for species or applications to receive product credits and other incentives. This program is available for scientists worldwide. Read on to discover the various applications for PRDX1.

P16/CDK6/cyclin D1 pathway

PRDX1 is a molecule that regulates the cell cycle. It has several functions, including regulating cell growth and death. By regulating the cell cycle, PRDX1 regulates autophagy. It also affects the PTEN-AKT signaling pathway. Its upregulation is an effective therapeutic strategy for the treatment of nephropathy associated with diabetes.

Regulation of lipophagic flux

PRDX1 is an important regulator of lipophagy and is essential for oxidative stress-induced atherosclerosis. It regulates lipophagy by scavenging ROS and is expressed at high levels in macrophages. It is essential for maintaining cholesterol homeostasis in macrophages and may be a promising therapeutic target for atherosclerosis and other autophagy-related diseases.

Autophagy is a recycling process initiated by cells in response to oxidative stress. Autophagy involves the release of ROS, which attack key cellular macromolecules, including protein cysteinyl thiols. Autophagy also removes bulky organelles and restricts ROS production. Despite these benefits, autophagy is still under intense oxidative regulation.

Inhibition of tubular senescence by PRDX1

The PRDX1 marker is involved in the regulation of cell cycle and senescence. It regulates the expression of p16, cyclin D1, IL-6, and TGF-b1. Its phosphorylation inhibits peroxidase activity. When knocked down, RTECs show a senescent phenotype. Inhibition of PRDX1 by DcR2 is effective in inhibiting DN.

To understand its function in cell cycle regulation, PRDX1 was first studied in DN. It is predominantly expressed in RTECs and STZ mice. It regulates cell cycle by interacting with cyclin-dependent kinases 4, 6, and p16. It also participates in cellular senescence through the p16 pathway.

A major role in the progression of DN is played by premature senescence of renal cells. Researchers found that PRDX1 regulates the phosphorylation of DcR2, a cell cycle-related protein that contributes to renal fibrosis and DN. Moreover, it is a potential target for therapeutic agents that target the clearance of senescent cells.

Several miRNAs have been implicated in oxidative stress-induced senescence. Further, miRNAs modulate the levels of key senescence effectors. These miRNAs recognize complementary sequences in the 3'UTRs of targeted mRNAs and function with a sequence-specific silencing mechanism. These miRNAs have conserved target sequences across mammalian species. They also affect signaling networks implicated in redox homeostasis and stress responses. As a result, cellular redox status could regulate the biogenesis of miRNAs.

Molecular clone-based assays of the PRDX1 marker show that a significant reduction in RTEC activity is associated with decreased expression of the PRDX1 gene. These studies also reveal a role for PRDX1 in the suppression of tubular senescence. As more evidence is gathered, researchers can use the PRDX1 marker to test the efficacy of cellular anti-aging agents.

Inhibition of senescence by PRDX1 requires the presence of the DNMT3A gene. Its RNA-binding site is enriched in miR-29a-3p and miR-30c-5p, which repress DNMT3A expression. Both miR-21a and miR-30c were associated with reductions in ROS, improved SOD2 protein levels, and enhanced mitochondrial functions.