Targeting protein kinase C subtypes in pancreatic cancer

Störz, Peter

doi:10.1586/14737140.2015.1003810

Cited by 17 publications

(13 citation statements)

References 49 publications

(50 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Conversely, Atf3 –/– acinar cells maintained accumulation of these junctional markers 4 h ( Figure 6A ) into CIP, suggesting that the mature acinar cell phenotype is maintained in these animals. IF analysis for atypical PKCζ, a marker of cell polarity that regulates junctional formation ( Storz, 2015 ), also revealed maintained accumulation only in Atf3 –/– tissue during CIP ( Figure 6B ). Cell–cell junction organization and cell junction assembly were identified in our GO analysis as targets of ATF3 regulation (Supplemental Table S2).…”

Section: Resultsmentioning

confidence: 89%

Activating transcription factor 3 promotes loss of the acinar cell phenotype in response to cerulein-induced pancreatitis in mice

Fazio

Young

Toma

et al. 2017

MBoC

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 89%

Activating transcription factor 3 promotes loss of the acinar cell phenotype in response to cerulein-induced pancreatitis in mice

Fazio

Young

Toma

et al. 2017

MBoC

View full text Add to dashboard Cite

show abstract

“…However, recent studies show that, at least in vitro, PRKCA has a specific function in tumor suppression [ 156 ]. The complex role of PKC in cancer may reflect the complicated interactive relationship between PRKCA and PC [ 156 , 158 ]. All in all, our predicted gene PRKCA has been confirmed to be definitely associated with pancreatic cancer, while, at the same time, the various functions of PRKCA imply the complex role of such gene in pancreatic cancer.…”

Section: Resultsmentioning

confidence: 99%

Mining for Candidate Genes Related to Pancreatic Cancer Using Protein-Protein Interactions and a Shortest Path Approach

Yuan

Zhang

Wan

et al. 2015

BioMed Research International

View full text Add to dashboard Cite

Pancreatic cancer (PC) is a highly malignant tumor derived from pancreas tissue and is one of the leading causes of death from cancer. Its molecular mechanism has been partially revealed by validating its oncogenes and tumor suppressor genes; however, the available data remain insufficient for medical workers to design effective treatments. Large-scale identification of PC-related genes can promote studies on PC. In this study, we propose a computational method for mining new candidate PC-related genes. A large network was constructed using protein-protein interaction information, and a shortest path approach was applied to mine new candidate genes based on validated PC-related genes. In addition, a permutation test was adopted to further select key candidate genes. Finally, for all discovered candidate genes, the likelihood that the genes are novel PC-related genes is discussed based on their currently known functions.

show abstract

“…The protein kinase C (PKC) family consists of ubiquitously expressed homologous serine/threonine kinases, which are divided into three groups according to their second messenger requirements: classical, novel, and atypical [40–43]. Classical PKCs consist of α, β I , β II , and γ isoforms and require Ca 2+ , diacylglycerol (DAG), phosphatidylserine, and phorbol esters for activation.…”

Section: Role Of the Pkc Family In Ec Dysfunctionmentioning

confidence: 99%

“…Atypical PKCs consist of ζ and ι/λ isoforms, and they lack the calcium-sensitive C2 domain and contain only one atypical C1 domain. Thus, atypical PKCs are unresponsive to DAG and calcium [40–43]. …”

Section: Role Of the Pkc Family In Ec Dysfunctionmentioning

confidence: 99%

Flow signaling and atherosclerosis

Sandhu

Quintana-Quezada

et al. 2016

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Atherosclerosis rarely develops in the region of arteries exposed to undisturbed flow (u-flow, unidirectional flow). Instead, atherogenesis occurs in the area exposed to disturbed flow (d-flow, multidirectional flow). Based on these general pathohistological observations, u-flow is considered to be atheroprotective, while d-flow is atherogenic. The fact that u-flow and d-flow induce such clearly different biological responses in the wall of large arteries indicates that these two types of flow activate each distinct intracellular signaling cascade in vascular endothelial cells (ECs), which are directly exposed to blood flow. The ability of ECs to differentially respond to the two types of flow provides an opportunity to identify molecular events that lead to endothelial dysfunction and atherosclerosis. In this review, we will focus on various molecular events, which are differentially regulated by these two flow types. We will discuss how various kinases, ER stress, inflammasome, SUMOylation, and DNA methylation play roles in the differential flow response, endothelial dysfunction, and atherosclerosis. We will also discuss the interplay among the molecular events and how they coordinately regulate flow-dependent signaling and cellular responses. It is hoped that clear understanding of the way how the two flow types beget each unique phenotype in ECs will lead us to possible points of intervention against endothelial dysfunction and cardiovascular diseases.

show abstract

Targeting protein kinase C subtypes in pancreatic cancer

Cited by 17 publications

References 49 publications

Activating transcription factor 3 promotes loss of the acinar cell phenotype in response to cerulein-induced pancreatitis in mice

Activating transcription factor 3 promotes loss of the acinar cell phenotype in response to cerulein-induced pancreatitis in mice

Mining for Candidate Genes Related to Pancreatic Cancer Using Protein-Protein Interactions and a Shortest Path Approach

Flow signaling and atherosclerosis

Contact Info

Product

Resources

About