Difference between revisions of "Part:BBa K3450001"
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β-catenin is a human transcription factor responsible for effecting pro-survival and pro-proliferative signals downstream of the Wnt signalling cascade, through its Wnt-dependent protection from the cell’s proteasomal machinery. This feature can be exploited to ensure the cell-specific retention of proteins it is fused to, since protein fusions containing β-catenin are only stable in cells that receive and transduce Wnt signals, such as actively cycling stem cell niches. | β-catenin is a human transcription factor responsible for effecting pro-survival and pro-proliferative signals downstream of the Wnt signalling cascade, through its Wnt-dependent protection from the cell’s proteasomal machinery. This feature can be exploited to ensure the cell-specific retention of proteins it is fused to, since protein fusions containing β-catenin are only stable in cells that receive and transduce Wnt signals, such as actively cycling stem cell niches. | ||
It is to be noted, however, that the specificity of its retention can be hindered by N-terminal fusions, since its own N-terminus is responsible for interactions with the factors that degrade it. | It is to be noted, however, that the specificity of its retention can be hindered by N-terminal fusions, since its own N-terminus is responsible for interactions with the factors that degrade it. | ||
Revision as of 18:04, 23 October 2020
Beta Catenin: Transcription factor and an effector of the Wnt signalling pathway.
β-catenin is a human transcription factor responsible for effecting pro-survival and pro-proliferative signals downstream of the Wnt signalling cascade, through its Wnt-dependent protection from the cell’s proteasomal machinery. This feature can be exploited to ensure the cell-specific retention of proteins it is fused to, since protein fusions containing β-catenin are only stable in cells that receive and transduce Wnt signals, such as actively cycling stem cell niches.
It is to be noted, however, that the specificity of its retention can be hindered by N-terminal fusions, since its own N-terminus is responsible for interactions with the factors that degrade it.