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Involved in pre-mRNA alternative splicing regulation. Additionally we are shipping MBNL1 Antibodies (105) and and many more products for this protein.
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Depletion of Mbnl1 and/or Mbnl2 (show MBNL2 Proteins) reduced localization of hundreds of transcripts, implicating Mbnls in localization of mRNAs to neurites
Sense DMPK (show DMPK Proteins) RNA foci clearly co-localize with MBNL1 and MBNL2 (show MBNL2 Proteins) 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 Proteins) 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
MBNL1 overexpression may be a valuable strategy for treating the skeletal muscle features of Myotonic dystrophy .
Nuclear retention of full-length HTT (show HTT Proteins) RNA is mediated by splicing factors MBNL1 and U2AF65 (show U2AF59 Proteins)
muscleblind-like 1 (MBNL1) is a robust suppressor of multiorgan breast cancer metastasis. It binds the 3' untranslated regions of DBNL (show DBNL Proteins) and TACC1 (show TACC1 Proteins) -two genes that are implicated as metastasis suppressors.
abnormal splicing of DMD (show DMD Proteins) exon 78 found in dystrophic muscles of DM1 (show DMPK Proteins) patients is due to the functional loss of MBNL1 and leads to the re-expression of an embryonic dystrophin (show DMD Proteins) in place of the adult isoform.
Reduced RBFOX1 (show A2BP1 Proteins) 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 Proteins)-1307 leading to low expression of miR (show MLXIP Proteins)-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 (Drosophila)
, muscleblind-like protein 1
, muscleblind-like 1
, triplet-expansion RNA-binding protein