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Basic helix-loop-helix (bHLH) transcription factors such as MyoD, E12, and E47 are key regulators of gene expression and control many differentiation events during development [ 1- 3].
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As with many cell differentiation events, the differentiation of B cells to antibody-secreting plasma cells is believed to be a physiologically irreversible process.
Notch signaling defines a conserved, pleiotropic cell-interaction pathway that controls cell fates and consequently many differentiation, proliferation and apoptotic events throughout development [1] [3].
Moreover, many of these differences in gene expression appear to be associated with metamorphic differentiation events that are eminent in met1 mex/Att hybrids, but not met1 mex/mex hybrids.
This marks the beginning of major differentiation events.
As Notch has been shown to induce early differentiation events and has been linked to cell cycle withdrawal, it is possible that diminished Notch receptor expression is common to many hyperproliferative skin disorders rather then specific to AD.
It is interesting to note that many differentiation protocols and technologies for cellular analysis require cell dissociation but have failed to recognize the potent bioactivity associated with this event (for example [42]).
Skeletal morphogenesis directs such differentiation events in space and time.
p57kip2 plays a role in many biological events including differentiation, apoptosis, cell-proliferation and tumorigenesis.
Apoptosis, the process of programmed cell death, is fundamental to many biological events, including development, differentiation, regulation of the immune system and cancer.
The dynamic chromatin landscape displaying combinatorial complexity of the epigenome impacts gene expression that underlies many events of differentiation and cell cycle progression.
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