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Involved in pre-mRNA alternative splicing regulation. Additionally we are shipping MBNL1 Antibodies (8) and many more products for this protein.
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Data show that Muscleblind-like 1 (Mbnl1) and Muscleblind-Like 3 (Mbnl3) bind skeletal muscle chloride channel CIC-1 (Clc-1) mRNA.
Depletion of Mbnl1 and/or Mbnl2 (show MBNL2 ELISA Kits) reduced localization of hundreds of transcripts, implicating Mbnls in localization of mRNAs to neurites
Sense DMPK (show DMPK ELISA Kits) RNA foci clearly co-localize with MBNL1 and MBNL2 (show MBNL2 ELISA Kits) proteins and accumulate in myotonic dystrophy 1 tissues during development.
MBNL1 overexpression promotes transformation of fibroblasts into myofibroblasts.
These data indicate that MBNL1 plays a conserved role in negatively regulating TGFbeta (show TGFB1 ELISA Kits) signaling, and is required for normal valve morphogenesis and homeostasis in vivo.
this study supports a key role for Mbnl1 loss in the initiation of DM1 cardiac disease.
Differential expression of Mbnl1 in development plays a role in alternative splicing of vesicular trafficking genes in postnatal heart development.
Results show that nuclear localization is a major determinant of MBNL1 function. It promotes the nuclear retention of repeat-containing transcripts, which results in repression of aberrant protein expression from the expanded repeats.
depletion of Mbnl proteins in mouse embryo fibroblasts leads to misregulation of thousands of alternative polyadenylation events.
consistent with a central and negative regulatory role for MBNL 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
Nuclear retention of full-length HTT (show HTT ELISA Kits) RNA is mediated by splicing factors MBNL1 and U2AF65 (show U2AF59 ELISA Kits)
muscleblind-like 1 (MBNL1) is a robust suppressor of multiorgan breast cancer metastasis. It binds the 3' untranslated regions of DBNL and TACC1 -two genes that are implicated as metastasis suppressors.
abnormal splicing of DMD (show DMD ELISA Kits) exon 78 found in dystrophic muscles of DM1 (show DMPK ELISA Kits) patients is due to the functional loss of MBNL1 and leads to the re-expression of an embryonic dystrophin (show DMD ELISA Kits) in place of the adult isoform.
Reduced RBFOX1 activity in myotonic dystrophy type 1 tissues may amplify several of the splicing alterations caused by the deficiency in MBNL1.
MBNL1 binds with C allelic pre-miR (show MLXIP ELISA Kits)-1307 leading to low expression of miR (show MLXIP ELISA Kits)-1307-3p in colorectal cancer.
The result is consistent with the hypothesis that MBNL proteins are trapped by expanded CUG repeats and inactivated in myotonic dystrophy type 1 (DM1) and that CELF1 is activated in DM1.
Results highlight the importance of RNA binding by MBNL Zinc Finger domains 1 and 2 for splicing regulatory activity, even when the protein is artificially recruited to its regulatory location on target RNAs.
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.
Involved in pre-mRNA alternative splicing regulation. Binds to CUG triplet repeat in RNA (By similarity).
, muscleblind-like protein 1
, triplet-expansion RNA-binding protein