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Fig. 3 — RNA splicing and splicing regulator changes in prostate cancer pathology.

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paper figure Created: 2026-04-21T18:29:40 By: paper_figures_tool Quality: 50% 🔗 External ID: paper-fig-paper-6ec76a6d668d-3
Fig. 3 — RNA splicing and splicing regulator changes in prostate cancer pathology.
Fig. 3Figure 3
Transcriptional control by a the full-length androgen receptor and b constitutively active AR isoforms made by splice variants. In ( a ), testosterone enters the prostate cancer cell and becomes modified to dihydroxytestosterone (DHT) by 5α-reductase. DHT binds to the androgen receptor (AR), displacing heat shock protein 90 (HSP) and resulting in AR translocation into the nucleus. Once inside the nucleus, the AR binds to consensus DNA sequence elements called androgen response elements (AREs) to control target gene expression. In ( b ), an androgen receptor variant protein (AR-V) lacking the ligand-binding domain is able to directly translocate into the nucleus without binding to DHT, resulting in androgen-independent control of gene expression
PubMed: paper-6ec76a6d668d
Metadata
pmidpaper-6ec76a6d668d
captionTranscriptional control by a the full-length androgen receptor and b constitutively active AR isoforms made by splice variants. In ( a ), testosterone enters the prostate cancer cell and becomes m
image_urlhttps://www.ebi.ac.uk/europepmc/articles/PMC5602090/bin/439_2017_1792_Fig3_HTML.jpg
paper_titleRNA splicing and splicing regulator changes in prostate cancer pathology.
figure_labelFig. 3
figure_number3
_schema_version1
source_strategypmc_api
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