March 13, 2017 Parallel
cellular pathways activate the process that controls organ growth A new study from the University of Chicago suggests that while proteins that control organ growth accumulate around the edges of cells, they actually function at a different cellular site.
Not exact matches
G protein - coupled receptors (GPCRs) are actually a huge protein family (i.e., superfamily) of transmembrane receptors that sense molecules outside Eukaryotic Cells in species ranging from yeast to humans, and
activate very basic biological
pathways and
cellular responses inside the cells.
In this new paper, the researchers reveal more about that mechanism, showing that without the protective ability of BRCA1, breaks in the DNA strands go unfixed, prompting the molecule ATM kinase to
activate a
cellular «suicide»
pathway involving a protein called p53.
The damage that it will repair is the one that is causal in senenscence of DNA
pathway (such x-ray radiation causing senescence) and oncogenic
activated senescence; but not of the type of replicative senescence (that's the domain of telomeres / telomerase / sub-telomeres and epigenetics) and
cellular replication / proliferation.
The model will describe
cellular pathways that contribute to tumor formation and explain in detail how the genetic disposition of an individual can
activate expression of genes that drive uncontrolled cell growth and lead to cancer.
This understanding of the
cellular and molecular mechanism of recovery from acute promyelocytic leukaemia opens prospects for
activating this same PML / p53
pathway in other types of cancers.
Insulin is not needed for protein synthesis or to
activate the mTOR
pathway, that causes
cellular growth.
Reactive oxygen species trigger
cellular responses by activation of stress - responsive mitogen -
activated protein kinase (MAPK) signalling
pathways.