Evidence map›Paper›PMID 27109495›Full record

ArticleHistochemistry and cell biology2016

HEK293 cells express dystrophin Dp71 with nucleus-specific localization of Dp71ab.

Atsushi Nishida, Sato Yasuno, Atsuko Takeuchi, Hiroyuki Awano, Tomoko Lee, Emma Tabe Eko Niba, Takahiro Fujimoto, Kyoko Itoh, Yasuhiro Takeshima, Hisahide Nishio and 1 more

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Article in Histochemistry and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

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  9. Cancer cell international · 2017
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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Atsushi NishidaDepartment of Physical Therapy, Faculty of Rehabilitation, Kobe Gakuin University, 518 Arise, Ikawadani, Nishi, Kobe, 651-2180, Japan.
Sato YasunoDepartment of Physical Therapy, Faculty of Rehabilitation, Kobe Gakuin University, 518 Arise, Ikawadani, Nishi, Kobe, 651-2180, Japan.
Atsuko TakeuchiKobe Pharmaceutical University, Higashinada, Kobe, 658-8558, Japan.
Hiroyuki AwanoDepartment of Pediatrics, Graduate School of Medicine, Kobe University, Chuo, Kobe, 650-0017, Japan.
Tomoko LeeDepartment of Pediatrics, Hyogo College of Medicine, Mukogawacho, Nishinomiya, 663-8501, Japan.
Emma Tabe Eko NibaDepartment of Physical Therapy, Faculty of Rehabilitation, Kobe Gakuin University, 518 Arise, Ikawadani, Nishi, Kobe, 651-2180, Japan.
Takahiro FujimotoDepartment of Pathology and Applied Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, 602-8566, Japan.
Kyoko ItohDepartment of Pathology and Applied Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, 602-8566, Japan.
Yasuhiro TakeshimaDepartment of Pediatrics, Hyogo College of Medicine, Mukogawacho, Nishinomiya, 663-8501, Japan.
Hisahide NishioDepartment of Community Medicine and Social Healthcare Science, Graduate School of Medicine, Kobe University, Chuo, Kobe, 650-0017, Japan.
Masafumi MatsuoDepartment of Physical Therapy, Faculty of Rehabilitation, Kobe Gakuin University, 518 Arise, Ikawadani, Nishi, Kobe, 651-2180, Japan. mmatsuo@reha.kobegakuin.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dystrophin gene consists of 79 exons and encodes tissue-specific isoforms. Mutations in the dystrophin gene cause Duchenne muscular dystrophy, of which a substantial proportion of cases are complicated by non-progressive mental retardation. Abnormalities of Dp71, an isoform transcribed from a promoter in intron 62, are a suspected cause of mental retardation. However, the roles of Dp71 in human brain have not been fully elucidated. Here, we characterized dystrophin in human HEK293 cells with the neuronal lineage. Reverse transcription-PCR amplification of the full-length dystrophin transcript revealed the absence of fragments covering the 5' part of the dystrophin cDNA. In contrast, fragments covering exons 64-79 were present. The Dp71 promoter-specific exon G1 was shown spliced to exon 63. We demonstrated that the Dp71 transcript comprised two subisoforms: one lacking exon 78 (Dp71b) and the other lacking both exons 71 and 78 (Dp71ab). Western blotting of cell lysates using an antibody against the dystrophin C-terminal region revealed two bands, corresponding to Dp71b and Dp71ab. Immunohistochemical examination with the dystrophin antibody revealed scattered punctate signals in the cytoplasm and the nucleus. Western blotting revealed one band corresponding to Dp71b in the cytoplasm and two bands corresponding to Dp71b and Dp71ab in the nucleus, with Dp71b being predominant. These results indicated that Dp71ab is a nucleus-specific subisoform. We concluded that Dp71, comprising Dp71b and Dp71ab, was expressed exclusively in HEK293 cells and that Dp71ab was specifically localized to the nucleus. Our findings suggest that Dp71ab in the nucleus contributes to the diverse functions of HEK293 cells.

Indexed as

Cell NucleusDystrophinHEK293 CellsHumansProtein Isoformsapo-dystrophin 1DystrophinProtein IsoformsDp71Dp71abDystrophinHEK293 cellsNucleus

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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.