DUSP2 Antibodies

Dual specificity protein phosphatase 2 (DUSP2)

Regulates mitogenic signal transduction by dephosphorylating both Thr and Tyr residues on MAP kinases ERK1 and ERK2. .

Gene Information

Human
Gene Name:	DUSP2
Uniprot:	Q05923
Entrez:	1844

Family

Belongs to:
protein-tyrosine phosphatase family

Alternative Names

dual specificity protein phosphatase 2; PAC-1; dual specificity phosphatase 2; PAC1

Molecular Weight

Mass (kDA):
34.4 kDA

Genomic Context

Human
Location:	2q11.2
Sequence:	2; NC_000002.12 (96143166..96145468, complement)

Tissue Specificity

Expressed in hematopoietic tissues.

Subcellular Localizations

Nucleus.

Diseases

• Neoplasms
• Inflammation
• Malignant Neoplasms
• Hemorrhage
• Tissue Adhesions
• Cardiovascular Diseases
• Thrombosis
• Coronary Artery Disease
• Hypoxia
• Pituitary Diseases
• Infarction
• Inflammatory Response
• Myocardial Infarction

• Bleeding Tendency
• Melanoma
• Tumor Angiogenesis
• Lymphoma
• Rheumatoid Arthritis
• Postoperative Hemorrhage
• Angina Pectoris

Pathways

• Platelet Activation
• Platelet Aggregation
• Secretion
• Cell Proliferation
• Coagulation
• Immune Response
• Inflammatory Response
• Hemostasis
• Localization
• Cell Adhesion
• Proteolysis
• Hypersensitivity
• Cell Cycle

• Angiogenesis
• Pathogenesis
• Cell Activation
• Gene Silencing
• Osteoblast Differentiation
• B Cell Activation
• Cell Cycle Arrest

PTMs

• Phosphorylation
• Dephosphorylation
• Cleavage
• Demethylation

• Nitration
• Carboxylation
• Biotinylation
• Methylation

• Palmitoylation

Research Areas

• Signal Transduction

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/DUSP2

Best Uses Of The DUSP2 Marker From Boster Bio

If you're interested in using the DUSP2 marker in your research, you've come to the right place. Boster offers high-affinity primary antibodies that have been validated for use in Western Blotting, Immunohistochemistry, and ELISA. Their reagents have been widely used within the research community and are of high quality. Here are some of these most popular uses for the DUSP2 marker.

DUSP2 Marker

Hypoxia treatment reversed the decrease in DUSP2 protein levels and mRNA levels in cancer cell lines. Inhibition of DUSP2 caused prolonged ERK phosphorylation, increased chemoresistance, and reduced cell growth and survival. Inductions in DUSP2 were associated with drug sensitivity and tumor progression. DUSP2 is also known to negatively regulate a variety of genes including those involved in drug resistance, cell survival, angiogenesis, and cell response. This makes DUSP2 an important target for developing novel molecular therapies.

These results indicate that the marker may be useful in identifying cancer stem cell. Hypoxia encourages the accumulation CSC in colorectal and other forms of cancer. Hypoxia can also lead to an increase in prostaglandin E 2 production (PGE), which can promote cancer stemness. These conditions can be treated by using inhibitors of PGE 2 signal transduction or biosynthesis. These inhibitors also inhibit hypoxia-induced tumorsphere growth and inhibit the synthesis COX-2.

It is still not clear what role DUSP2 has in regulating inflammation. Overexpression of DUSP2 causes an increase in inflammation. This is true for autoimmune disorders and HIV infection. Loss-of-DUSP2 promotes lymphangiogenesis. Although its role in pancreatic carcinoma research is still limited it is a promising tool for therapeutic and diagnostic purposes.

DUSP2 is an important gene in the epithelial-mesenchymal transition process. This gene has been linked with the ability of cancer cell to migrate on a hard surface. Knockdown DUSP2 induced formation of a tumorsphere. However, DUSP2 inducing its expression in primary colorectal cells inhibits this process. These results are however limited by the DUSP2 proteins, which are not expressed in epithelial cell cells.

DUSP2 downregulation may also improve the sensitivity to chemotherapy drugs. Researchers collected gene-expression data from 688 colorectal cancer patients. They found a strong correlation between DUSP2 activity and COX-2 expression (Supplementary Fig. S4D). Hypoxia also increased the CD44+/CD133+ levels and promoted the formation a tumorsphere.

DUSP2 is downregulated by most cancer cells, but it can be a valuable marker for cervical epithelial and colon cells. Moreover, DUSP2-KD tumours exhibited increased lymphangiogenesis and nodal metastasis. These findings suggest that the loss of DUSP2 could play an important part in the initiation, progression, and treatment of cancer. These findings need to be confirmed clinically.

Moreover, DUSP2 transiently expressed decreased levels of VEGF C in pancreatic carcinoma cells. Moreover, DUSP2 transiently expressed decreased secreted VEGF –C and EV VEGF –C. These findings demonstrate the utility of using DUSP2 to diagnose. These findings support the idea that DUSP2 can be used as a biomarker for pancreatic carcinoma.

DUSP proteins target MAPKs and signaling nodes and have become a versatile regulator of T cell biology. The dual specific phosphatases (DUSPs) target MAPKs and signaling nodes, and have a diverse range of applications. Here are the most commonly used DUSP2 markers. What are the Best Uses For DUSP2

Regulation of DUSP2 via miR-361-3p

This study found that miR-3611-3p expression was present in HepG2 or Huh7 cells when they were cultured in DMEM with 10% Fetus serum, 2 M L-glutamine, 25 ug/ml Gentamicin, and DMEM. It was found to be negatively correlated with CD24/CD133 expression in HCC tissues. It was also upregulated in liver TICs.

It has been shown that miR-361-3p plays a role in pancreatic carcinoma. These miRNAs consist of small, noncoding molecules with 22 nucleotides. MiRNAs regulate many physiological processes. Although its function remains unclear in many biological diseases and processes, it has been demonstrated to promote tumor survival in human breast cancer cells and liver-T-ICs. DUSP2 promotes the survival of cells that undergo the epithelial-to-mesenchymal transition, a key process in solid tumor metastasis.

Despite being complex, miR-361-3p plays important roles in many kinds of cancers. It regulates genes that regulate the immune system and tumor growth. It has also been shown that it regulates the CX-C motif chemokine receiver 6 (STAT6). Ma et. The study by Ma and al.

These results suggest that miR-361-3p is a fundamental regulator in non-small-cell lung carcinoma and esophageal cancer. Its role in pancreatic carcinoma remains unknown. This study was done to determine the role of miR-361, which is responsible for controlling cell migration and viability. It also revealed that miR-361 mimic significantly decreased pancreatic cells proliferation and increased apoptosis among PC cells.

The results showed miR-361-3p directly targeted SOX1 liver T-ICs. Sox1 3'UTR was mutated, (MUT), which led to decreased mRNA levels. Western blot showed that miR-3611-3p negatively correlated to SOX1 expression in clinical samples. The molecule miR-3611-3p targets SOX1 and is therefore an important regulator of immune system.

Moreover, miR-361-3p is known to directly regulate the protein OSR2 and Bax in BCPAP cells. Luciferase reporter tests have confirmed that miR-3631-3p interacts with hsa_circ_0011385. The miR-361-3p mimic significantly attenuated the luciferase activity induced by wild-type Hsa-circ_0011385, but the effect was reversed by siRNA. Further, miR-361-31p was shown positive to regulate OSR2.

MiR-361-3p also decreased the expression levels of PC tumor cells and increased sensitivity for sorafenib, cisplatin, and cisplatin. These findings suggest that miR-361 could be used to diagnose and predict HCC patients. For data, the author is available. The datasets are available on reasonable request. There are no overlapping studies in literature on the role miR-361 plays in cancer.

These results suggest that miR-361-3p regulates MAPK/JNK transcription. The miR-361 knockdown MAPK/JNK by MiR-361 is associated both with apoptosis and tumor growth in cancer cells. Moreover, it has been shown to inhibit metastasis. But further research is needed to confirm these findings. In the meantime miR-3611-3p expression is reduced in human cells.

Expression of DUSP2 during pancreatic Cancer

DUSP2 is a tumor suppressor that blocks the activity of its physiological substrate ERK2. This pathway is responsible both for cell proliferation and survival. Phosphorylation of ERK1/2 leads to cellular growth. Cancer cells that express DUSP2 more often have a higher risk of developing Pancreatic Cancer. This suggests that the pathway may act as a gatekeeper.

The DUSP2 genes is expressed in both cancerous and healthy cells. A reduction in its expression will cause a decrease in prognosis. Pancreatic cancer can be caused by deletion of this gene. However, it is not known if DUSP6 has been mutated. A decrease in DUSP6 expression can be associated with constitutive activation MAPK1/ERK2. Alternatively, overexpression of DUSP6 causes dephosphorylation of MAPK1, leading to the suppression of proliferation and eventual apoptosis.

Additionally, DUSP2 promoter DNA methylation was associated with decreased DUSP2 gene expression in human cancer cells. This methylation is associated with transcriptional silencing in cancer cells. Moreover, DUSP2 expression has been shown to correlate with poorer overall survival in serous ovarian cancer. Further research is needed to confirm if DUSP2 can suppress tumours.

Pancreatic cancer cells have shown that DUSP2 overexpression can inhibit cell migration and increase expression of ERK1/2. Furthermore, DUSP2 expression inversely correlates with ERK1/2 phosphorylation in pancreatic cancer cells. Clinical samples have confirmed that the inhibitory effects miR-361-3p has on DUSP2 expression in pancreatic carcinoma cells and the co-IP test have shown positive results.

The loss of DUSP2 in pancreatic cancer cells has also been shown to increase the activity of proprotein convertase 2 (PPC) and vesicle trafficking in PDAC, suggesting that the loss of DUSP2 may be a significant factor in the early dissemination of pancreatic cancer. This discovery could prove to be useful in the development of novel therapies for pancreatic carcinoma.

As previously described, immunohistochemical analysis for DUSP2 was performed. Paraffin-embedded section were stained with specific antibodies (anti DUSP2, sc-32776 Santa Cruz and anti-E-cadherin. Vimentin, VEGF-C, Vimentin and N-cadherin were used to count cells in five randomly chosen microscopic areas. GraphPad Prism 6.01 software was used as a data analysis tool. One-way ANOVA was used to determine statistical significance, while Student t-test was used to evaluate statistical significance.

The activation of the apoptotic signaling pathway is activated in pancreatic Cancer by miR-3631-3p in combination with KRAS mutations. Inactive MAPK induces many genes and miRNAs involved in malignant tumor phenotypes. This may offer a new therapeutic approach for pancreatic cancer treatment by blocking the functions of the induced genes.

MKPX/DUSP2 is primarily located in the nucleus. However they are not implicated in cancer. Genetic studies have found increased mRNA levels in hepatomas, pancreatic cancer, familial modulatory thyroid carcinoma, and multiple endocrine neoplasia. Mice lacking MKP–DUSPs also have impaired adaptive and innate immune responses.