TXNRD2 Antibodies

Thioredoxin reductase 2, mitochondrial (TXNRD2)

Involved in the management of reactive oxygen species levels and the regulation of mitochondrial redox homeostasis (PubMed:24601690). Maintains thioredoxin in a reduced state.

May play a role in redox-regulated cell signaling. .

Gene Information

Human
Gene Name:	TXNRD2
Uniprot:	Q9NNW7
Entrez:	10587

Family

Belongs to:
class-I pyridine nucleotide-disulfide oxidoreductase family

Alternative Names

EC 1.8.1; EC 1.8.1.9; KIAA1652; Selenoprotein Z; SelZ; Thioredoxin Reductase 2; thioredoxin reductase 3; thioredoxin reductase beta; Thioredoxin reductase TR3; TR; TR3; TR-beta; TRXR2; TRXR2thioredoxin reductase 2, mitochondrial; TXNRD2

Molecular Weight

Mass (kDA):
56.507 kDA

Genomic Context

Human
Location:	22q11.21
Sequence:	22; NC_000022.11 (19875518..19941818, complement)

Tissue Specificity

Highly expressed in the prostate, ovary, liver, testis, uterus, colon and small intestine. Intermediate levels in brain, skeletal muscle, heart and spleen. Low levels in placenta, pancreas, thymus and peripheral blood leukocytes. According to PubMed:10608886, high levels in kidney, whereas according to PubMed:9923614, levels are low. High expression is observed in the adrenal cortex (PubMed:24601690).

Subcellular Localizations

Mitochondrion.

Diseases

• Malignant Neoplasms
• Malignant Neoplasm Of Breast
• Neoplasms
• Mammary Neoplasms
• Cardiomyopathy, Dilated
• Hypoxia
• Digeorge Syndrome
• Malignant Neoplasm Of Prostate
• Cardiomyopathies
• Ataxia
• Heart Failure
• Prostatic Neoplasms

• Colorectal Neoplasms
• Colorectal Cancer
• Schizophrenia
• 22q11 Deletion Syndrome
• Hyperplasia
• Congenital Cerebellar Hypoplasia
• Stomach Neoplasms

Pathways

• Cell Proliferation
• Cell Growth
• Aging
• Cell Death
• Translation
• Cognition
• Prepulse Inhibition
• Regeneration
• Pathogenesis
• Transport
• Programmed Cell Death
• Electron Transport
• Brain Development

• Oxidative Phosphorylation
• Inflammatory Response
• Cell Division
• Regulation Of Histone Acetylation
• Cell Cycle
• Histone Acetylation
• Response To Superoxide

PTMs

• Reduction
• Oxidation

• Phosphorylation
• Cleavage

• Acetylation

Research Areas

• Breast Cancer
• Membrane Trafficking and Chaperones

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TXNRD2

Best Uses Of The TXNRD2 Marker

His bio may interest you if you're interested in learning more about Steven Boster. This article will provide information about Boster's life, philosophy, achievements, and background. Then you can decide if you want to buy the TXNRD2 mark. This marker requires a special type or tagging system.

History of Steven Boster

This page will provide information about Steven Boster’s history. Boster's public records include his current and past addresses as well as his mobile phone numbers, email addresses, and mobile phone numbers. You can also find out if Boster had any relatives. To learn more about Boster’s background, you can filter your search using age, state and more. In just minutes, you can access public records about Steve Boster.

Steve Boster, 60 years old, died peacefully on June 6, 2022. He was born in Joliet (IL) and died after a long battle fighting COVID-19. His two daughters, Crystal Boster and Natosha Peck, are his survivors, as well his six grandchildren. He was also survived by four siblings, Jack Boster, Sandra Blanton and Tammy. Boster also leaves many nieces, nephews.

His achievements

Gasdaska and colleagues discovered that the TXNRD2 gene may reduce oxidative stress in cells by inhibiting the opening of the mitochondrial permeability transition port. How does this protein accomplish this? What are its biological functions, then? This study reveals its intricate workings. Let's take a look at some of its functions.

His philosophy

Mutagenesis of a corresponding gene is one way to investigate TXNRD2's gene. Site-directed PCR mutation was performed using a pGEM–T-Easy–Txnrd2 template. To create an Ala-T mutation, we used the Ala codeon in Txnrd2. To make a G375R mutagenesis, we changed Gly to Arg.