With regard to the potential role of PKD in myocardium, recent observations raise the possibility that PKD-mediated myocardial regulatory mechanisms may represent promising therapeutic avenues for the treatment of heart failure.
With regard to the potential role of PKD in myocardium, recent observations raise the possibility that PKD-mediated myocardial regulatory mechanisms may represent promising therapeutic avenues for the treatment of heart failure.
While myocardial infarction is a possible complication of atheroscletotic coronary aneurysms, it is reasonable to assume that CA in patients with PKD may make them prone for a similar complication.
While it is expressed in most tissues in the normal state, PKD1 expression may increase or decrease during tumorigenesis, and its role in proliferation is context-dependent and poorly understood.
Whereas the direct activation of mTOR has been shown recently in autosomal-dominant PKD, no data are available on the role of mTOR signalling in proliferation and progression of ARPKD.
We identified novel PKD1 inhibitors and assessed their antitumor activity <i>in vitro</i> in TNBC cell lines and <i>in vivo</i> in a TNBC patient-derived xenograft (PDX) model.
We identified novel PKD1 inhibitors and assessed their antitumor activity <i>in vitro</i> in TNBC cell lines and <i>in vivo</i> in a TNBC patient-derived xenograft (PDX) model.
We have reported an important role for PKD in stimulated peptide secretion from a human (BON) carcinoid cell line; however, the role of PKD isoforms, including PKD2, in the proliferation and invasion of carcinoid tumors remains unclear.
We conclude that chronic upregulation and activation of inositol trisphosphate receptors, CaMKII, and PKD in HF shifts HDAC5 out of the nucleus, derepressing transcription of hypertrophic genes.
We conclude that chronic upregulation and activation of inositol trisphosphate receptors, CaMKII, and PKD in HF shifts HDAC5 out of the nucleus, derepressing transcription of hypertrophic genes.
We also found that reduction of PRKD1 by ectopic miR-34a expression or PRKD1 siRNA treatment resulted in suppressed self-renewal ability in breast cancer stem cells.
We also found that reduction of PRKD1 by ectopic miR-34a expression or PRKD1 siRNA treatment resulted in suppressed self-renewal ability in breast cancer stem cells.
Using an animal model, we show that reversion of PRKD1 promoter methylation with the DNA methyltransferase inhibitor decitabine restores PKD1 expression and blocks tumor spread and metastasis to the lung in a PKD1-dependent fashion.