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HighlightsTumor suppressor candidate 3 (TUSC3) is a putative tumor suppressor located at chromosomal region 8p22. It is often lost in epithelial cancers, such as prostate, breast, oral squamous, pancreatic, colorectal or ovarian cancer. TUSC3 is localized to the endoplasmic reticulum in an oligosaccharyl tranferase complex responsible for the N-glycosylation of proteins. Together with magnesium transporter 1 (MAGT1) and non-imprinted in Prader-Willi/Angelman syndrome region protein 2 (NIPA2), TUSC3 is deeply involved in vertebrate plasma membrane transport of Mg2+. It has been found to modulate intracellular Mg2+ concentrations in a human cell line and is pivotal for many biochemical functions and morphological and cytological changes. Epigenetic silencing of TUSC3 has been associated with poor prognosis.
| Basic Information of TUSC3 | |
| Protein Name | Tumor suppressor candidate 3 |
| Gene Name | TUSC3 |
| Aliases | Magnesium uptake/transporter TUSC3, Protein N33, N33 |
| Organism | Homo sapiens (Human) |
| UniProt ID | Q13454 |
| Transmembrane Times | 4 |
| Length (aa) | 348 |
| Sequence | MGARGAPSRRRQAGRRLRYLPTGSFPFLLLLLLLCIQLGGGQKKKENLLAEKVEQLMEWSSRRSIFRMNGDKFRKFIKAPPRNYSMIVMFTALQPQRQCSVCRQANEEYQILANSWRYSSAFCNKLFFSMVDYDEGTDVFQQLNMNSAPTFMHFPPKGRPKRADTFDLQRIGFAAEQLAKWIADRTDVHIRVFRPPNYSGTIALALLVSLVGGLLYLRRNNLEFIYNKTGWAMVSLCIVFAMTSGQMWNHIRGPPYAHKNPHNGQVSYIHGSSQAQFVAESHIILVLNAAITMGMVLLNEAATSKGDVGKRRIICLVGLGLVVFFFSFLLSIFRSKYHGYPYSDLDFE |
TUSC3 has also been identified as a potential tumor suppressor gene. Defects in TUSC3 caused by deletions or mutations are frequently associated with mental retardation. In prostate, breast, oral squamous, pancreatic, colorectal or ovarian cancer, TUSC3 is significantly down-regulated in tumor tissues. Homozygous deletion of TUSC3 and epigenetic regulation of TUSC3 expression through promoter methylation are considered to be potential aetiological factors related to tumor dissemination and progression. According to the Oncomine database, the expression of TUSC3 gene is significantly downregulated in patients with ovarian cancer, indicating a potential clinical relevance of TUSC3 in the pathogenesis of ovarian cancer. Moreover, epigenetic silencing of TUSC3 has been associated with poor prognosis of ovarian cancer, and hypermethylation of its promoter provides an independent biomarker of overall and disease-free survival in ovarian cancer patients.
Fig.1 Model for TUSC3 functions in CRC. (Burgermeister, 2017)
The article confirms the tumor-suppressive function of TUSC3 and identifies the possible mechanism driving TUSC3-deficient ovarian cancer cells toward a malignant phenotype.
The article reports that the reduction of immunological TUSC3 staining is a prognostic factor for the low survival rate of patients with pancreatic cancer. The decreased of TUSC3 can promote pancreatic cancer cell proliferation, invasion, and metastasis.
The results of this article show that TUSC3 may be responsible for alternations in the proliferation ability, aggressiveness, and invasive/metastatic potential of colorectal cancer.
The article reveals that TUSC3 regulates proliferation and invasion of glioblastoma multiform cells by inhibiting the activity of the Akt signaling pathway.
Authors in this group found that N33/Tusc3 increased glycosylation efficiency for a subset of human glycoproteins by slowing glycoprotein folding.
To obtain the soluble and functional target protein, the versatile Magic™ membrane protein production platform in Creative Biolabs enables many flexible options, from which you can always find a better match for your particular project. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-TUSC3 antibody development services.
As a leading service provider, Creative Biolabs is proud to present our professional service in membrane protein preparation and help you with the research of membrane proteins. Please do not hesitate to inquire us for more details.
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