TGM2 Antibodies

Protein-glutamine gamma-glutamyltransferase 2 (TGM2)

Catalyzes the cross-linking of proteins and the conjugation of polyamines to proteins. .

Gene Information

Human
Gene Name:	TGM2
Uniprot:	P21980
Entrez:	7052

Family

Belongs to:
transglutaminase superfamily

Alternative Names

C polypeptide; EC 2.3.2.13; G-ALPHA-h; protein-glutamine gamma-glutamyltransferase 2; protein-glutamine-gamma-glutamyltransferase; TG(C); TG2; TGase C; TGase H; TGase-2; TGase-H; TGC; TGCGNAH; TGM2; Tissue transglutaminase; transglutaminase 2 (C polypeptide, protein-glutamine-gamma-glutamyltransferase); Transglutaminase 2; Transglutaminase C; Transglutaminase H; transglutaminase-2; tTG

Molecular Weight

Mass (kDA):
77.329 kDA

Genomic Context

Human
Location:	20q11.23
Sequence:	20; NC_000020.11 (38127385..38166508, complement)

Diseases

• Malignant Neoplasms
• Neoplasms
• Neoplasm Metastasis
• Malignant Neoplasm Of Lung
• Cell Invasion
• Tissue Adhesions
• Carcinoma
• Malignant Neoplasm Of Breast
• Malignant Paraganglionic Neoplasm
• Neoplasm Invasiveness
• Inflammation
• Cell Transformation, Neoplastic
• Lung Neoplasms

• Malignant Neoplasm Of Ovary
• Malignant Neoplasm Of Pancreas
• Nerve Degeneration
• Schizophrenia
• Glaucoma, Open-angle
• Fibrosis
• Mammary Neoplasms

Interacting Proteins

• AKAP13
• APP
• COL18A1
• FN1
• KRT19

• LOX
• RELA
• VHL

Pathways

• Pathogenesis
• Methylation
• Secretion
• Cell Adhesion
• Cell Migration
• Proteolysis
• Wound Healing
• Oncogenesis
• Cell Proliferation
• Insulin Secretion
• Localization
• Drug Resistance
• Keratinization

• Synapse Organization
• Ossification
• Cell Cycle Arrest
• Inflammatory Response
• Histone H4 Acetylation
• Reverse Transcription
• Chemotaxis

PTMs

• Methylation
• Amidation
• Demethylation
• Acetylation

• Deamidation
• Biotinylation
• Phosphorylation
• Reduction

• Deacetylation

Research Areas

• Apoptosis
• Immune System Diseases
• Immunology
• Signal Transduction

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TGM2

Best Uses Of The TGM2 Marker

In this article, we'll look at the TGM2 marker as a new molecular marker that has recurrence risk and early prognostication for disease. We'll also discuss the ways in which the TGM2 marker acts as a target for epigenetic silencing. We'll also examine some of the most effective applications of the TGM2 marker.

TG2 is an molecular marker that is a first

Transglutaminase is a general, crosslinking enzyme controlled by redox potential, Ca2+ and Guanine Nucleotides. TG2 is a scaffold protein in cells, and is typically elevated in response to stressors from the environment and external. This enzyme is also an anti-tumor agent. The TG2 molecule is an important part of the cell's defense mechanisms.

We found that TG2 overexpression facilitated the differentiation into neurons of EMSCs. Transfected with TG2, EMSCs showed a higher proportion of Ki-67+ cell lines and significantly improved differentiation into neurons. The TG2-EMSCs also were able to express Tuj-1, GAP43 and MAP2 antigenic marker. These molecules were also more readily expressed by Western Blotting.

Our research also revealed that breast cancer cells expressing TG2 undergo EMT which is a process that promotes drug resistance. Stable TG2 expression also induces EMT which leads to the loss of epithelial markers and the growth of mesenchymal markers. Interestingly, TG2 also increases the expression of transcription repressors, which are known to promote EMT.

TG2 is the cell's primary driver for differentiation and functions as an adhesion receptor to laminin or fibronectin. In vivo and in vitro, TG2 is involved in various processes, including cell differentiation and growth. It has also been associated with neuroblastoma SH-SY5Y cell. These cells have been the subject of extensive research in primary cultures.

TG2 was expressed in EMSCs through transfection using an Adenoviral vector. Ad-EMSCs were also used as control. In all experiments, TG2 expression was significantly higher after adenoviral transduction compared to without TG2.

TG2 is also implicated in the growth of tumors in the spinal cord and brain. Extracellular TG2 is a stabilizing agent that helps promote protein synthesis in ECM components. This could contribute to the aggressiveness of tumors due to altered cell-cell interactions. In addition, TG2 regulates cell adhesion and integrin-mediated signaling on the cell surface. It also works with integrin receptors, as well as fibronectin.

Transglutaminase 2 is an enzyme involved in cross-linking proteins via (g-glutamyl) Lysine bonds. The enzyme has been shown to be elevated in patients with renal cancer, and CHIP, which functions as an E3 ubiquitin ligase encourages polyubiquitination of TG2. It also helps reduce tumor growth by lowering TG2.

It's a prognostic indicator for early disease Recurrence

TGM2 is a brand-new protein that has important physiological and pathological roles. It is more abundantly expressed during the activation of hepatic stellate cell stellate cells and the their differentiation into muscle fibroblasts. The levels of its expression are connected to the onset of cancer and atherosclerosis. TGM2 protein levels were found to be high in malignant tumors, as well as metastatic lung cancer cells.

Researchers from Ningxia Medical University, Yunchuan (China) recently examined 42 patients with colorectal carcinoma. They were able to compare TGM2 levels in normal tissues, and then analysed the levels of expression. Results of the study showed that the expression of TGM2 was significantly higher in tumor tissues than in adjacent normal tissues. Researchers also found an increase in Caspase-3 protein levels in patients who had received TGM2-siRNA.

A study of mice and TGM2-siRNA interference revealed that TGM2 also inhibited the expressions of crucial factors that contribute to the development of cancerous colon cells. TGM2-siRNA, created through a siRNA procedure, was proven to inhibit tumor growth and Wnt3a/bcatenin expression. Furthermore, it inhibited the expression of Caspase-1, MMPs, and the Wnt/b-catenin pathway.

Utilizing a single-cell transfection the cells were incubated with TGM2-siRNA or control-siRNA. The transfection was performed using the reagent (CCK-8) manufactured by Beyotime, China. The cells were then incubated for 12, 24 and 48 hours, after which they were analyzed for apoptosis levels using the flow cytometer and CellQuest Pro software.

Recent research using siRNA-based technologies showed that the transfection of TGM2-siRNA can reduce the viability of colorectal carcinoma cells. The study involved 42 patients. While the RNA-siRNA treatment increased tumorigenesis in mice, the results indicated that TGM2-siRNA-transfection reduced overall survival rate. This study has significant implications for treatment of colorectal cancer and research.

In addition to the immune system, Boster Bio also provides high-affinity primary antibodies that are verified in numerous research studies. Boster Bio's antibodies have been frequently used in scientific research for more than 25 years. They have been used for immunohistochemistry, ELISA, and Western Blotting. Further, the anti-TGM2-recombinant antibody was able to detect TGM2 in TGM2-positive cancer tumors, which is a significant prognostic factor in early disease recurrence.

It is a goal of epigenetic silencing

The TGM2 gene has emerged as a possible target to epigenetic silencing in breast cancer. This molecular event that is out of the ordinary is recognized to negatively regulate PI3K/AKT signaling and is also associated with the activity of tumor suppressors in both colon cancers of the human species and liver cancer. Epigenetic silencing of the TGM2 gene is among several promising approaches to combating breast cancer.

Multiple cancers, including colon and leukemia have been proven to be influenced by epigenetic methylation. It has been proven to induce various tumor-suppressor genes, such as p53 C-Myc, and Cyclophosphamide. Different epigenetic mechanisms have proven to increase TG2 expression including DNA methylation.

HDAC inhibitors, in addition to their ability to target TGM2, are extremely effective. They are able to be combined to stimulate gene expression in a synergistic manner. In an investigational trial in Phase I that included valproic acids and 5-azacitidine, they together resulted in a stable disease state for up to 12 months in a select group of patients. These epigenetic silencing proteins could be accessed by chemotherapy agents, which could lead to better tumor suppression.

To determine whether TG2 is a potential epigenetic target, scientists performed several experiments to determine TG2 level of mRNA as well as the activity of transglutaminase in lung cancer cells. The most effective method used was siRNA transfection. It caused apoptosis to A549 cells. SimiRNA transfection also increased ROS levels. Additionally, TG2 knockdown reduced ROS-induced AKT activation and superoxide dismutase 2.

TG2 knockdown triggers apoptosis in H2299 and A549 cells. It also leads to high levels of cleaved PARP and apoptosis associated caspases (H2299 cells). In A549 cells the knockdown of TG2 causes an apoptosis. These results are further confirmed by an immunoblot analysis.