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However the mechanisms whereby the Mbnl proteins mediate these functions and the role of these novel functional aspects of the Mbnl proteins in disease initiation has yet to be fully understood.
However, the interactions that mediate these functions are not known.
The molecular mechanisms by which CDKs mediate these functions are unknown.
Despite growing evidence of the diverse functions of Bergmann glia, the molecular mechanisms that mediate these functions have remained largely unknown.
DCC and CEACAM1 contribute to the adhesive, migratory, or invasive properties of several types of solid tumor cells [13] [16] including neuroblastoma [17], but the molecular interactions that mediate these functions have been difficult to identify.
Therefore, we hypothesized that RBPs may, as a group, be extensively regulated to mediate these functions.
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MiR-210 mediates these functions by regulating a lot of target mRNAs.
Htl is involved in mediating these functions (Franzdottir et al. 2009).
It mediates these functions via binding to its unique receptor c-Met, a receptor tyrosine kinase.
miR-210 mediates these functions by regulating a lot of target mRNAs.
Functional studies showed that these mutant receptors retain DNA binding but exhibit significant impairment of transcriptional activation and coactivator recruitment in response to different ligands (Barroso et al., 1999; Agostini et al., 2004), due to the mutations destabilizing the carboxyterminal α helix of PPARγ (Kallenberger et al., 2003), which mediates these functions.
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