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The release of sequences -- not the virus itself, but the pattern of amino acids in its genes, which shows what mutations it has made -- is a touchy subject because some scientists try to keep the data secret until they can publish scientific papers.
Even though the molecules and processes involved in replicating the genome function very efficiently to reduce the number of mutations, it has been observed that errors still arise during genome duplication [1].
Although a number of cancer genes contribute to tumorigenesis in a manner of co-occurring or anti-co-occurring mutations, it has been challenging to gain a global landscape of when, where, and how their interactions exert affects on tumor formation and development.
After the discovery of CALR mutations, it has been proposed to be mutually exclusive with JAK2 and MPL mutations in MPN.
Based on this, for all three studied mutations, it has been evaluated the frequency of false positive calls measured as the percentage of erroneously called bases at the target site.
In melanomas, which also harbour BRAFV600E mutations, it has been demonstrated that BRAFV600E activates the MAPK pathway and controls proliferation of melanoma cells through the regulation of cyclin D1 and of the cyclin-dependent kinase inhibitor p27Kip1 [ 4- 7].
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In the case of the Arctic mutation, it has been reported that aggregates (oligomer, protofibrils, and fibril) formed by this mutation are indistinguishable to those formed by Wild Type under free solution conditions [51].
Because A1 is a de novo mutation, it has an initial frequency of p0 = 1/(2 N).
If one ISC acquires a neutral mutation it has a high risk of being replaced by a normal stem cell within the crypt.
Although it is recognised that the BRAF mutation is not a UV-signature mutation, it has been suggested that it could still arise due to error-prone reduplication of UV-damaged DNA (Thomas et al, 2006).
Bradi4g09420 contains the two R mutations, but in place of the active site mutation, it has a large deletion through the chitin-binding domain, entirely eliminating the DXXDXDXE motif in this protein.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com