ArticleEndocrine
Prolactin-regulated pim-1 transcription: identification of critical promoter elements and Akt signaling.
Article in Endocrine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- The Human Intermediate Prolactin Receptor I-tail Contributes Breast Oncogenesis by Targeting Ras/MAPK Pathway.Endocrinology · 2024Article
- Effects of sustained hyperprolactinemia in late gestation on the mammary parenchymal tissue transcriptome of gilts.BMC genomics · 2023Article
- Breast Cancer and Prolactin - New Mechanisms and Models.Endocrinology · 2022Review
- The Role of PIM Kinases in Pediatric Solid Tumors.Cancers · 2022Review
- PIM1 Inhibition Affects Glioblastoma Stem Cell Behavior and Kills Glioblastoma Stem-like Cells.International journal of molecular sciences · 2021Article
- Expressions of Osteopontin (OPN), ανβ3 and Pim-1 Associated with Poor Prognosis in Non-small Cell Lung Cancer (NSCLC).Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2012Article
- Article
- Coordinated expression of tristetraprolin post-transcriptionally attenuates mitogenic induction of the oncogenic Ser/Thr kinase Pim-1.PloS one · 2012Article
- Myocardial AKT: the omnipresent nexus.Physiological reviews · 2011Review
- Why target PIM1 for cancer diagnosis and treatment?Future oncology (London, England) · 2010Review
- Mitochondrial integrity: preservation through Akt/Pim-1 kinase signaling in the cardiomyocyte.Expert review of cardiovascular therapy · 2009Review
- Nuclear and mitochondrial signalling Akts in cardiomyocytes.Cardiovascular research · 2009Review
- PIM-1-specific mAb suppresses human and mouse tumor growth by decreasing PIM-1 levels, reducing Akt phosphorylation, and activating apoptosis.The Journal of clinical investigation · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Previously we showed that the distal element (DE) (-427 to -336 bp) within the pim-1 promoter appeared to regulate its prolactin (PRL)-induced transcription. To determine which specific DE sequences conferred PRL responsiveness, seven 12-bp deletion mutants ligated upstream of the chloramphenicol acetyltransferase gene were transfected into FDC/Nb2 cells. Results from promoter/ reporter studies showed that sequential 12-bp deletions of the DE significantly (p < 0.001) reduced PRL responsiveness. An additional site, nuclear factor-1 (-224 to -217), was also mutated by deletion or point mutation; both abrogated promoter activation by PRL (p < 0.0001). In other experiments, PRL signaling to pim-1 expression was investigated in FDC/Nb2 cells stably expressing the wild-type (WT) Jak2 cDNA or a carboxy-terminal kinase-deficient Jak2 mutant and in cells infected with adenoviral constructs of WT-Akt or dominant negative Akt. Altered Jak2 did not affect PRL-stimulated pim-1 expression while inhibition of Akt attenuated its transcription. We conclude that the DE and NF-1 half-site mediate PRL responsiveness of the pim-1 promoter. Moreover, the accumulated evidence does not support a role for the Jak2/Stat signaling pathway but, instead, implicates that Akt activation was a component of PRL-induced pim-1 transcription.
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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.