TP63 Break Apart FISH Probe
€0.00
In stock
SKU
TP63BA-20-
Catalog Number: TP63BA-20-
Size: 20 tests (40 μl)
€ 50,00 order handling applies
Size: 20 tests (40 μl)
€ 50,00 order handling applies
The TP63 Break Apart FISH Probe is used to detect TP63 gene aneusomy. Order a custom TP63 Break Apart FISH probe labeled in Orange, Green, Red, Gold or Aqua and receive it in as little as 7 business days.
TP63 is a gene that codes for the tumor protein P63, a transcription factor that directs the activity of a wide variety of effector genes. It regulates functions crucial to early development, from proliferation and differentiation to cell adhesion and apoptosis1. These mechanisms function at large in the growth of limbs, organs, body systems, and facial features. TP63 remains important throughout life, too – in humans that’ve reached full maturity, it continues to regulate cell genesis and death, so can also be thought of as a kind of life span monitor1.
Because of its role in cell growth and maintenance, abnormalities in TP63 can have devastating physical effects, with ectodermal dysplasia, orofacial clefting and limb malformations being the most common2. Although mutations in the gene’s DNA binding domain appear to be the root of most of the aforementioned physical abnormalities, TP63 translocations have been found to contribute to the development of lymphomas and some lung adenocarcinomas, among other cancers3. Shuffling of the gene also helps to further characterize the nature of the disease. For example, TP63 jumping in ALK-negative anaplastic large-cell lymphoma, although rare, is correlated with more aggressive disease progression4.
Because the gene’s movement is more difficult to track than its absence or overexpression, the oncongenic nature of TP63 translocations aren’t as well understood. TPG3 jumping, therefore, will likely be the subject of plenty of cancer-related studies in the future.
Loci: 3q28
TP63 is a gene that codes for the tumor protein P63, a transcription factor that directs the activity of a wide variety of effector genes. It regulates functions crucial to early development, from proliferation and differentiation to cell adhesion and apoptosis1. These mechanisms function at large in the growth of limbs, organs, body systems, and facial features. TP63 remains important throughout life, too – in humans that’ve reached full maturity, it continues to regulate cell genesis and death, so can also be thought of as a kind of life span monitor1.
Because of its role in cell growth and maintenance, abnormalities in TP63 can have devastating physical effects, with ectodermal dysplasia, orofacial clefting and limb malformations being the most common2. Although mutations in the gene’s DNA binding domain appear to be the root of most of the aforementioned physical abnormalities, TP63 translocations have been found to contribute to the development of lymphomas and some lung adenocarcinomas, among other cancers3. Shuffling of the gene also helps to further characterize the nature of the disease. For example, TP63 jumping in ALK-negative anaplastic large-cell lymphoma, although rare, is correlated with more aggressive disease progression4.
Because the gene’s movement is more difficult to track than its absence or overexpression, the oncongenic nature of TP63 translocations aren’t as well understood. TPG3 jumping, therefore, will likely be the subject of plenty of cancer-related studies in the future.
Loci: 3q28
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