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MBNL2 is a member of the muscleblind protein family which was initially described in Drosophila melanogaster. De plus, nous expédions MBNL2 Protéines (6) et beaucoup plus de produits pour cette protéine.
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Mbnl1 (Montrer MBNL1 Anticorps)(+/-); Mbnl2(+/-) knockout mice with myotonic dystrophy presented with clinical myofibril ultrastructural abnormality and cardiac arrhythmias.
Depletion of Mbnl1 (Montrer MBNL1 Anticorps) and/or Mbnl2 reduced localization of hundreds of transcripts, implicating Mbnls in localization of mRNAs to neurites
Sense DMPK (Montrer DMPK Anticorps) RNA foci clearly co-localize with MBNL1 (Montrer MBNL1 Anticorps) and MBNL2 proteins and accumulate in myotonic dystrophy 1 tissues during development.
depletion of Mbnl (Montrer MBNL1 Anticorps) proteins in mouse embryo fibroblasts leads to misregulation of thousands of alternative polyadenylation events.
consistent with a central and negative regulatory role for MBNL (Montrer MBNL1 Anticorps) proteins in pluripotency, their knockdown significantly enhances the expression of key pluripotency genes and the formation of induced pluripotent stem cells during somatic cell reprogramming
This analysis identified several hundred splicing events whose regulation depended on Mbnl (Montrer MBNL1 Anticorps) function in a pattern indicating functional interchangeability between Mbnl1 (Montrer MBNL1 Anticorps) and Mbnl2.
We propose that major pathological features of the myotonic dystrophy brain result from disruption of the MBNL2-mediated developmental splicing program
Conserved developmental stage- and tissue-specific alternative splicing of MBNL (Montrer MBNL1 Anticorps) transcripts is an important mechanism by which MBNL (Montrer MBNL1 Anticorps) activity is regulated during embryonic development.
The authors propose that expanded CTG DNA repeats cause two separate effects: loss of Mbnl1 (Montrer MBNL1 Anticorps) function (disrupting splicing) and loss of another function that disrupts extracellular matrix mRNA regulation, possibly mediated by Mbnl2.
MBNL2 contribute to the pathogenesis of myotonic dystrophy.
MBNL2 in splicing regulation of specific transcripts, which, when altered, contributes to the myotonic dystrophy phenotype.
both MBNL1 and MBNL2 are involved in the regulation of Tau exon 2 splicing and the mis-splicing of Tau in DM1 is due to the combined inactivation of both
MBNL (Montrer MBNL1 Anticorps) proteins promote opposite splicing patterns for cardiac troponin T (Montrer TNNT2 Anticorps) and insulin receptor (Montrer INSR Anticorps) alternative exons
MBNL1 (Montrer MBNL1 Anticorps) and MBNL2 always co-distributed. Functional differences between MBNL1 (Montrer MBNL1 Anticorps) and MBNL2 have not yet been found
solution structures of both tandem zinc finger (TZF (Montrer Znf318 Anticorps)) motifs, TZF12 (comprising ZF1 (Montrer PRMT1 Anticorps) and ZF2 (Montrer ZNF274 Anticorps)) and TZF34 (ZF3 and ZF4), in MBNL2
This gene is a member of the muscleblind protein family which was initially described in Drosophila melanogaster. This gene encodes a C3H-type zinc finger protein that modulates alternative splicing of pre-mRNAs. Muscleblind proteins bind specifically to expanded dsCUG RNA but not to normal size CUG repeats and may thereby play a role in the pathophysiology of myotonic dystrophy. Several alternatively spliced transcript variants have been described but the full-length natures of only some have been determined.
muscleblind-like protein 2
, muscleblind-like 2
, muscleblind-like protein 1
, muscleblind-like protein-like 39