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1 Citations
Facts about Tartrate-resistant acid phosphatase type 5.
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Human | |
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Gene Name: | ACP5 |
Uniprot: | P13686 |
Entrez: | 54 |
Belongs to: |
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metallophosphoesterase superfamily |
ACP5; TRACP; TRACP-5b; TTRRAP
Mass (kDA):
36.599 kDA
Human | |
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Location: | 19p13.2 |
Sequence: | 19; NC_000019.10 (11574660..11578983, complement) |
Lysosome.
Are you curious about the Boster Bio: The Best Uses for the ACP5 Marker? Check out this article to learn about the marker and its functions. You will also learn more about Melanoma and TRAP. The Anti-Acid-Phosphatase/ACP5 Marker a highly relevant marker. It is used for the study of a range of diseases.
This new boster protein identifies the anti-acid-phosphatase/ACP5 enzyme found in human cells. The protein has several applications in the body and could assist researchers in determining the presence of an acid phosphatase enzyme within blood samples of patients. It was discovered that an anti-ACP5 protein with a high amount is vital for the proper functioning of the immune system.
The Boster Bio Antis-Acid Phosphatase/ACP5 is part of the Picoband(tm) catalog. This antibody reacts with human and mouse forms of this enzyme. Trehalose is also found in the antibody and has been confirmed by using negative and positive samples. While there are many other brand of antibodies with similar characteristics similar to the Boster brand however, it is most well-known for its high-affinity antibody.
ACP5 regulates the function of p53 within the cytoplasm by dephosphorylating Ser392 from the p53. In this way, it promotes p53 ubiquitination, which eventually leads to the degradation of. ACP5 also regulates signaling pathways between p53 and SMAD3, which is crucial in regulating EMT in cancer. These preliminary results suggest that there is lots of potential for this gene.
ACP5 is an enzyme that mature osteoclasts release. ACP5 activity in serum is used to evaluate osteolysis caused by metastasis of a few malignancies. ACP5 has also been demonstrated to promote liver cancer metastasis and the invasion of GC cells. A study of melanoma cells found that ACP5 increased expression is associated with decreased autophosphorylation focal adhesionkinase (FAK) located at Tyr3, which promotes cancer cell invasion. ACP5 overexpression in melanoma was also associated with an increase in cancer cell movements, morphological changes and autophosphorylation of focal adsorption kinase (FAK) at Tyr3.
These studies were done using GEM models that were able to identify genes that control invasion and transformation. To identify genes with high biological significance Genomic homogeneity was utilized between different GEM tumors. Cross-species comparisons were also used. The analysis of gene expression revealed that 360 genes were expressed in a different way and this was linked to the metastatic potential for melanoma. This study offers new insights into the biology of melanoma , and how ACP5 is related to metastasis.
A number of recent studies have proven the importance of ACP5 to the development of cancer. Melanoma cells are known for their ability to overexpress ACP5 , which can promote invasion and growth. ACP5 expression may also contribute to cancer metastasis and tumorigenesis. ACP5 is a potential therapeutic agent for melanomas. More research is required in order to determine the function of ACP5 in the treatment of colorectal cancer.
ACP5 is a marker of melanocytes that contribute to the progression of melanoma. Melanoma cells create pigment, called melanin. Melanoma cells can develop into tumors if melanocytes cease producing this pigment. In an experimental assay for metastasis, ACP5 knockdown significantly reduced tumor growth in mice. ACP5 knockdown in mice with melanomas cells (green fluorescent protein) prevented the growth of tumors.
In a study of 170 GC patients, ACP5 expression was associated with a lower survival rate. Additionally, patients with low ACP5 expression had a higher chance of survival. This study suggests that ACP5 could be a biomarker for familial malignant melanoma. This research should continue. However, there are other environmental and genetic factors that can contribute to the development of melanoma.
The ACP5 protein interacts in the cytoplasm and with p53. It dephosphorylates Ser392 from luad cells. This triggers the ubiquitination and degradation of the protein. Furthermore, ACP5 blocks the repressive effect of p53 on SMAD3 which is a key transcriptional element in tumors. Targeting ACP5 therapeutically may be a good strategy to LUAD treatment.
ACP5 is elevated in breast cancer, hepatocellular cancer, ovarian cancer, and melanoma. It is useful in detecting bone metastasis, which is a characteristic of human melanomas. Additionally, it has been implicated in EMT. However, its role in tumor pathogenesis is not fully understood.
ACP5 increases EMT by dephosphorylating Ser392 P53 and stimulating ubiquitination. ACP5 additionally enhances the functions of SMAD3 in lung adenocarcinoma cells by regulating the SMAD3/p53 signaling. This suggests that ACP5 could increase EMT in lung cancer cell cells.
The ACP5 protein is a biomarker for tartrate-resistant acid phosphatase. Its presence in blood is associated with the risk of developing bone metastasis, which is a major cause of death. Further research is required to fully understand the function of ACP5 in bone metastasis. There are numerous uses for the ACP5 protein in bone metastasis.
PMID: 2909539 by Ketcham C.M., et al. Molecular cloning of the type 5, iron-containing, tartrate-resistant acid phosphatase from human placenta.
PMID: 2338077 by Lord D.K., et al. Type 5 acid phosphatase. Sequence, expression and chromosomal localization of a differentiation-associated protein of the human macrophage.
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