ArticleMolecular biology reports2026
Mutation of leucine 170 alters the subcellular distribution, neurite outgrowth and three-dimensional structure of dystrophins Dp71 and Dp40.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundIn addition to progressive muscle wasting, one-third of patients with Duchenne muscular dystrophy (DMD) exhibit varying degrees of cognitive impairment, which are associated with mutations of the DMD gene within the region coding for dystrophins Dp71 and Dp40. A previous study reported that the deletion of leucine 3238 in dystrophin Dp427 induces cognitive impairments without muscular dystrophy. This mutation has implications for all dystrophins, including Dp71 and Dp40.
objectiveThis study aimed to evaluate the effect of the deletion of leucine 170 (leucine 3238 in the full-length dystrophin Dp427) on the subcellular localisation, neurite outgrowth and three-dimensional (3D) structure of Dp71 and Dp40 isoforms.
methodsPC12 Tet-On cells were transiently transfected with pTRE2pur-Myc/Dp71 or Dp40 vectors, and recombinant Myc-Dp71/Dp40 proteins were expressed by adding doxycycline. The analysis of undifferentiated and nerve growth factor- (NGF) differentiated cells was conducted by cell morphology, immunofluorescence staining and confocal microscopy. The length of the neurites of differentiated cells was obtained using ImageJ software. Analyses of 3D models were carried out by Alphafold 2.0 and TM-align tools.
resultsOur research revealed that the deletion of leucine 170 (ΔL170) disturbs the membrane localisation and promotes the cytoplasm and nuclear accumulation of Dp71 and Dp40 in undifferentiated and NGF-differentiated PC12 Tet-On cells. Furthermore, this mutation altered the neurite outgrowth of PC12 Tet-On cells. It is important to note that both the deletion of leucine 170 (ΔL170) and the mutation of leucine 170 to proline (L170P) result in alterations to the 3D structures of these dystrophins.
conclusionsThe loss or mutation of leucine 170 disturbs the subcellular localisation, neuronal functions and 3D structures of Dp71 and Dp40. This may lead to cognitive deficits in patients with DMD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.