Sentence examples for mitochondrial entry from inspiring English sources
The translocase of the outer membrane (TOM) is a protein complex that forms the major mitochondrial entry site for precursor proteins synthesized in the cytosol.
The resultant MTS is cleaved on mitochondrial entry, such that the mature protein has the same molecular weight as in the nucleus [32].
For instance, mitochondrial entry and oxidation of free fatty acids regulated via the carnitine palmitoyltransferase (CPT) 1-dependent pathway has been associated to appetite regulation.
One was a MSA containing the same 1000 nucleotides of four genus Canis mitochondrial entries (AC numbers: NC_009686, NC_008092, NC_002008, NC_008093); this alignment only contained 18 divergent positions.
This is an electrophoretic process as the mitochondrial Ca2+ entry decreases the transmembrane potential and thus the uptake rate.
The identification of the channel responsible for mitochondrial Ca2+ entry, the Mitochondrial Ca2+Uniporter (MCU), together with its regulatory components, MICU1 and MCUR1, provides new molecular tools to investigate this process.
Where indicated, c-FLIP−/− cells were transiently transfected with pBluescript or c-FLIPL plasmids and mitochondrial Ca2+ entry were measured in Rhod-2AM-loaded cells.
Specifically, the suppression of mitochondrial Ca2+ entry by cancer-related miR-25 represents the first study of the control of the mitochondrial uniporter by miRNA and offers initial clues to the relevance of this pathway in human cancers.
Thus it is tempting to speculate that overexpression of Bcl-wav could lead to massive mitochondrial calcium entry and subsequent cell death which is inhibited by Nrz in zebrafish embryos.
Some 20 years ago we showed that adenine nucleotides could inhibit electrogenic mitochondrial K+ entry into mitochondria and that this was probably mediated by their binding to the ANT [49,186,187], in agreement with earlier proposals [188].
Despite c-FLIP−/− MEFs showed lower IP3- and TG-induced ER-to-cytosol Ca2+ release and mitochondrial Ca2+ entry than WT counterpart, such defects were not rescued by c-FLIPL re-introduction, suggesting possible additional mechanisms not directly relying on c-FLIP expression.
