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These findings indicate that N-linked oligosaccharides are required for holo-Tf-induced stabilization of hTfR2 and that no single N-linked site is responsible for the loss of responsiveness to Tf.
The cellular and molecular mechanisms underlying this loss of responsiveness are not clear.
Moreover, the cell line could be kept in culture for more than 1 month without a loss of responsiveness to general cellular stimuli.
Mutations in KRAS and p53 signaling pathways contribute to loss of responsiveness to current therapies and a decreased survival in lung cancer.
These lines have been maintained for several generations with no loss of responsiveness.
While PD-1 upregulation may contribute to loss of responsiveness, it certainly cannot explain it in entirety.
It has been demonstrated that this inability is caused by a loss of responsiveness to the chemical signal that induces sex [18].
Another explanation for the clear loss of tetramer+ populations, and loss of responsiveness associated with chronic infection would potentially be immune escape within the target epitope.
Maintenance of tissue homeostasis is a tightly regulated process and the loss of responsiveness to negative growth signals can alter this delicate balance, leading to cancer [1].
However, given that OP is a recessive trait involving a simple loss of function ( = loss of responsiveness to the sexual signal[18]), a mutation in a single gene is probably the most parsimonious explanation.
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Since MCF-7 cells retain estrogen responsiveness on Col I, we reasoned that LM signaling through α6 might be responsible for loss of estrogen responsiveness on LM.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com