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Preliminary work on computer modeling for pollen development and mutation will be described.
Mutation of D6 slowed tumor development, and mutation of S2 abrogated complementation activity.
BRCA1 and cyclin D1 are both essential for normal breast development and mutation or aberration of their expression is associated with breast cancer [ 1, 2].
A causal link between breast cancer development and mutation of ATM, BRCA1 and TP53 has been found in familial breast cancer syndromes (Buchholz et al, 1999).
p53 is a tumour suppressor protein that has a critical function in inhibiting cancer development, and mutation in the p53 pathway is an extremely common event in most human cancers.
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Complexes of postsynaptic neuroligins and LRRTMs with presynaptic neurexins contribute widely to excitatory synapse development, and mutations in these gene families increase the risk of developing psychiatric disorders.
The paired box gene 2 (PAX2) is a transcription factor expressed during embryonic eye development and mutations in the human and mouse homologs are accompanied by eye malformations [1].
LIN-12/Notch signaling is important for cell-cell interactions during development, and mutations resulting in constitutive LIN-12/Notch signaling can cause cancer.
This gene is essential for cartilage tissue development and mutations in it have been associated with Stickler syndrome type III and Marshall syndrome [46], which are characterized by hearing loss and bone and joint defects.
45 Sox10 plays a pivotal role in neural crest cell development, and mutations in Sox10 result in Waardenburg Shah syndrome.
Pax6 is crucial in eye development, and mutations in the insect and mammalian Pax6 homologues prevent eye development (reviewed by Gehring, 2002).
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