USP6 Break Apart FISH Probe
€0.00
In stock
SKU
USP6BA-20-
Catalog Number: USP6BA-20-
Size: 20 tests (40 μl)
€ 50,00 order handling applies
Size: 20 tests (40 μl)
€ 50,00 order handling applies
The USP6 Break Apart FISH Probe localizes to the USP6 gene allowing confirmation of rearrangements of the gene.
USP6 codes for the Ubiquitin Specific Peptidase 6 protein, which functions in removing ubiquitin from target proteins1. De-ubiquitination is a widely used post-transcriptional regulatory mechanism; its central purpose is to control protein stability in order to maintain normal chemical signaling and permeability in intercellular junctions2.
In normal cells, USP6 uses de-ubiquitination to drive important homeostatic processes, like DNA damage response, protein turnover, and vesicular trafficking, to name a few3. USP6’s cancer-causing properties were first discovered over 2 decades ago, when its translocation was found to promote pathogenesis in Ewing’s sarcoma2. USP6 rearrangements have also been found to contribute to tumor growth in the human neoplasms nodular fasciitis (NF) and aneurysmal bone cyst (ABC)1.
NF presents as a rapidly-growing, solitary soft tissue mass, generally occurring in adults ages 20-40 years old4. Although NF tumors are self-limiting and benign, they can be painful and obstructive if they push on nerves or bones4,5. USP6 is thought to stimulate NF by fusing with gene partners that promote transcriptional upregulation of USP6, which generates the soft tissue cell proliferation that leads to tumors5. ABC is a locally aggressive bone lesion that occurs primarily in the pediatric population6. USP6 promotes ABC tumor growth by largely the same mechanism as occurs in NF, moving to a novel promoter region that allows for overexpression of the gene6.
Loci: 17p13
USP6 codes for the Ubiquitin Specific Peptidase 6 protein, which functions in removing ubiquitin from target proteins1. De-ubiquitination is a widely used post-transcriptional regulatory mechanism; its central purpose is to control protein stability in order to maintain normal chemical signaling and permeability in intercellular junctions2.
In normal cells, USP6 uses de-ubiquitination to drive important homeostatic processes, like DNA damage response, protein turnover, and vesicular trafficking, to name a few3. USP6’s cancer-causing properties were first discovered over 2 decades ago, when its translocation was found to promote pathogenesis in Ewing’s sarcoma2. USP6 rearrangements have also been found to contribute to tumor growth in the human neoplasms nodular fasciitis (NF) and aneurysmal bone cyst (ABC)1.
NF presents as a rapidly-growing, solitary soft tissue mass, generally occurring in adults ages 20-40 years old4. Although NF tumors are self-limiting and benign, they can be painful and obstructive if they push on nerves or bones4,5. USP6 is thought to stimulate NF by fusing with gene partners that promote transcriptional upregulation of USP6, which generates the soft tissue cell proliferation that leads to tumors5. ABC is a locally aggressive bone lesion that occurs primarily in the pediatric population6. USP6 promotes ABC tumor growth by largely the same mechanism as occurs in NF, moving to a novel promoter region that allows for overexpression of the gene6.
Loci: 17p13
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