ArticleJournal of biosciences2014
Differential expression of speckled POZ protein, SPOP: putative regulation by miR-145.
Article in Journal of biosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- SPOP loss of function protects against tauopathy.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- c-Myb facilitates immune escape of esophageal adenocarcinoma cells through the miR-145-5p/SPOP/PD-L1 axis.Clinical and translational medicine · 2021Article
- SPOP Deregulation Improves the Radiation Response of Prostate Cancer Models by Impairing DNA Damage Repair.Cancers · 2020Article
- The diverse roles of SPOP in prostate cancer and kidney cancer.Nature reviews. Urology · 2020Review
- The emerging role of SPOP protein in tumorigenesis and cancer therapy.Molecular cancer · 2020Review
- SPOP and cancer: a systematic review.American journal of cancer research · 2020Review
- MicroRNA-5p and -3p co-expression and cross-targeting in colon cancer cells.Journal of biomedical science · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The speckle POZ protein, SPOP, is an adaptor of the Cul3-based ubiquitination process, and has been implicated in the carcinogenesis process. Despite recent elucidation of biological functions, regulation of SPOP gene expression has not been reported. In this study, the mRNA levels of the mouse SPOP (mSPOP) gene were first shown to vary noticeably in different tissues. However, the SPOP protein was detected in high abundance only in Purkinje cells of the cerebellum and seminiferous tubule of the testis, echoing previous reports of involvement of ubiquitination in neuron cells and in spermatogenesis. In other mouse tissues and human cancer cell lines analysed, only low SPOP protein levels were detected. The 3'-untranslated regions of both the mSPOP and human SPOP transcripts harbor a conserved putative miR-145 binding site (BS). In some tissues and cell lines, miR-145 and SPOP protein levels were in an inverse relationship suggesting miR-145 regulation. Luciferase assays of deletion and point mutation constructs of the miR-145 BS, and miR-145 induction by serum starvation that resulted in reduced endogenous SPOP levels provided further evidence that miR-145 is likely involved in post-transcriptional regulation of SPOP expression in selected tissues, and possibly with the participation of other miRNA species.
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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.