GSTA1 Antibodies

Glutathione S-transferase A1 (GSTA1)

Conjugation of reduced glutathione to a wide number of exogenous and endogenous hydrophobic electrophiles. .

Gene Information

Human
Gene Name:	GSTA1
Uniprot:	P08263
Entrez:	2938

Family

Belongs to:
GST superfamily

Alternative Names

EC 2.5.1.18; glutathione S-alkyltransferase A1; glutathione S-aryltransferase A1; glutathione S-transferase 2; glutathione S-transferase A1; glutathione S-transferase alpha 1; glutathione S-transferase Ha subunit 1; GST class-alpha member 1; GST HA subunit 1; GST, class alpha, 1; GST2; GSTA1-1; GST-epsilon; GTH1; MGC131939; S-(hydroxyalkyl)glutathione lyase A1

Molecular Weight

Mass (kDA):
25.631 kDA

Genomic Context

Human
Location:	6p12.2
Sequence:	6; NC_000006.12 (52791371..52803827, complement)

Tissue Specificity

Liver.

Subcellular Localizations

Cytoplasm.

Diseases

• Malignant Neoplasms
• Neoplasms
• Mammary Neoplasms
• Carcinoma
• Malignant Neoplasm Of Breast
• Liver Carcinoma
• Colorectal Cancer
• Colorectal Neoplasms
• Inflammation
• Carcinogenesis
• Adenocarcinoma
• Liver Neoplasms
• Malignant Paraganglionic Neoplasm

• Ovarian Neoplasm
• Prostatic Neoplasms
• Malignant Neoplasm Of Lung
• Malignant Neoplasm Of Prostate
• Venoocclusive Disease
• Dysequilibrium Syndrome
• Colonic Neoplasms

Pathways

• Conjugation
• Excretion
• Dna Repair
• Pathogenesis
• Transport
• Localization
• Cell Cycle
• Drug Resistance
• Cell Death
• Cell Proliferation
• Regeneration
• Aging
• Inflammatory Response

• Cell Growth
• Fibroblast Proliferation
• Fermentation
• Cell Differentiation
• Signal Transmission
• Cellular Localization
• Immune Response

PTMs

• Phosphorylation
• Acetylation
• Reduction

• Oxidation
• Glutathionylation
• Methylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/GSTA1

Best Uses of the GSTA1 Marker

In this article, we'll discuss the polymorphisms in the GSTA1 Marker, its applications in hepatocellular carcinoma, as well as its transfection efficacy. We'll also review its applications in different species, including humans. We'll also review the most effective uses of the GSTA1 Marker. These methods are useful to scientists across the globe. Continue reading to learn more.

GSTA1 Polymorphisms

There isn't any evidence that the GSTA1 gene is responsible for T2D but it could contribute to the risk of T2D. Despite this the fact that there are fewer GSTA1 polymorphisms in Caucasians than Africans. Furthermore, a study released last year showed that those who carry the GSTP1 Ile/Val (A/G) genotype had a lower chance of developing T2D.

GSTA1 is an enzyme belonging to the glutathione-s-transferase family. It plays an important role in detoxifying toxins as well as regulating cell signaling. However, only a tiny number of studies have looked into this enzyme's role in breast cancer. For instance, one study examined the relationship between GSTA1 polymorphisms and breast cancer, estrogen receptor status of tumors, and consumption of vegetables and fruits.

Despite these findings, however it isn't clear what the role GSTA1 is playing in the development of prostate cancer. While GSTA1 is implicated in the development of prostate tumors and prostate cancer, it isn't clear what role this enzyme plays in the pathology. It is not known how GSTA1 polymorphisms affect prostate health. In certain cases, however, it is found that its gene expression is elevated , and the presence of prostate cancer cells decreases. These results suggest that GSTA1 polymorphisms might play a role in the development of prostate cancer.

While the risk of developing gastric cancer is not entirely clear, research on GSTP1 polymorphisms could be a great first step towards the treatment of the disease. Moreover those with GSTT1 null genotypes were at greater likelihood of developing premalignant lesion. They did however have an extremely low risk of developing gastric cancer in the event that they carried a GSTP1Val gene.

While the risk of developing cervical cancer isn't affected by GSTA1 polymorphisms, it's important to know their effect on SCCA risk. In fact, a study conducted in the last few years discovered that GSTP1 G allele was associated with a lower risk of cervical cancer than the wild type homozygous individuals. Knowing your own GST genotype can help you reduce other risk factors.

The effects of genetic polymorphisms GSTA1 and GSTT1 genes on cancer risk have been examined in numerous studies. Mittal RD et al. examined the relationship between smoking and common GST polymorphisms and found that none were significantly associated with bladder cancer risk. Another study, Sivonova M., studied the polymorphisms in GSTM1 and GSTT1 in addition to the three types of GSTM1 and GSTP1 gene polymorphisms.

A study with KB-V1 cells discovered that GSTP1 silencing led to a 4-fold increase of DDP cytotoxicity. However, GSTA1 silencing resulted in the growth of DDP-resistant solid tumor cells. Additionally, GSTA1 silencing augmented the level of DDP cytotoxicity in KCNJ5 mutant cells, and increased the number of apoptotic cells within the SKOV3/A549 SKOV3/A549 DDP-resistant.

Applications of GSTA1 as biomarker in hepatocellular cancer.

In a study carried out on mice the low levels of GSTA1 are associated with a lower level of AFP and small tumor size and the presence of portal vein tumor thrombosis. GSTA1 was also linked to serum levels of liver-related pathological markers, like p-Akt or CDK6. The correlation was significant, but it is unclear whether the gene polymorphisms are related to clinical status, tumor size and Child-Pugh grade.

In mice, GSTA1 overexpression inhibited colony growth and invasion. Overexpression of GSTA1 also decreased expression of LKB1 and p-mTOR. These two kinases also reduced, which led to a decrease in tumor volume, weight, or OD450. These results suggest that GSTA1 could be a biomarker in the hepatocellular cancer.

Another study found that patients with HCC with higher levels of GSTP1 had higher survival rates. Patients with low levels GSTP1 had shorter OSs and DFSs, despite not having PVTT. Both groups had similar results, despite the differences in AFP, PVTT, and HCC subgroup. There is no definitive relationship between low levels of GSTP1 and survival in HCC, however.

The GSTA1 enzyme is part of a group of proteins called glutathione-S-transferases. They play a significant role in metabolism, detoxification carcinogenesis, and various other processes. In hepatic cancer, GSTA1 is a biomarker for cancer progression. A genetic polymorphism can detect the protein. However, it was not statistically significant in an older group.

The researchers investigated the GSTP1 gene polymorphisms of HCC patients as well as 386 healthy controls. The genetic polymorphism was linked to a higher risk of HCC. The researchers concluded that the polymorphism didn't affect the expression of other markers for clinical pathology. These findings are encouraging and will allow scientists to further study the genetic significance of GSTA1 in HCC.

In addition to being a significant biomarker for HCC, GSTP1 was associated with lower AFP levels and with better HCC outcomes. At the beginning of tumorigenesis tumours were smaller than in the later stages. However as the tumor expanded, the size increased. Although the levels in serum of AFP are a biomarker of HCC (although the specific mechanism isn't known) They do indicate that there may be some connection. While it's not certain if there is a link, it could suggest that GSTP1 may be involved in the growth and progression of HCC.

In the current study, we analyzed nine proteins that are associated with the HIF-1 pathway. We discovered that AUY922 treatment reduced the expression of nine proteins, including GSTA1. These 9 proteins can serve as potential markers for cancer. The study also provides proof of principle support for DIA-MS profiling using patient-derived models. This study makes it possible for the next generation proteomic strategy to be implemented by the field.

Transfection effectiveness of GSTA1

Recent research has revealed that siRNA targeting GSTA1 genes can increase the cytotoxicity of DDP. The IC50 of DDP was inversely correlated with the apoptotic percentage of cancer cells resistant to DDP. The most apoptotic percentage was observed when GSTA1 was shut down. In addition, the downregulation of GSTA1 expression could enhance DDP cytotoxicity.

The transfection efficiency of the GSTA1 gene was evaluated using a two-step approach. First, cells expressing GST are placed in 24-well plates. After 24 hours of incubation, cells were treated with 50% Methanol and DDP. The cells were then incubated for 72 hours with the mixture.

Another study revealed that siRNA targeting the GSTA1 gene decreased the cell apoptosis rate in DDP resistant cells. This could be due to the lower accuracy of western blots. Transfection of the GSTA1 gene to cancerous cells did not result in the expression of GSTA1. Despite these issues however, the study has been a source of hope that future research could be feasible.

SUN treatment increases an oxidative stress by altering the balance between production of free radicals and their elimination. SUN induced GSTa1 mRNA and protein levels in a concentration-dependent manner. It stimulated caspase-9, caspase-3, and inhibited apoptotic reactions. SUN produced ROS and enhanced GSTa1 expression. The rate of cell death in cells treated by SUN was about two-thirds lower.

Transfection of human HeK293T cells was made possible by the GSTA1 marker. This cell line has the ability to express functionally-normal detoxification enzymes, and is extensively employed in drug metabolism and toxicology studies. It is also appropriate for studying virus Adsorption and entry into host cells. Thus, it is possible to assess the effectiveness of GSTA1 transfection. Transfection of GSTA1 is an excellent option if you are looking to know the way GSTA1 regulates the immune system.

Quantitative RT-PCR was used to measure the GSTA1 mRNA expression levels. Using an Applied Biosystems QuantStudio Flex RT-PCR system, cDNA was subjected to PCR amplification. We employed SYBR Green Universal Master mix and a human primer purchased from Integrated DNA technologies. We also used a human bactin to fix the fold-change in gene expression.