Mode of Publication: Hybrid (Open Access & Subscription)
Peer Reviewed Journal
The journal Cell Biology: Research & Therapy (CBRT) promotes rigorous research that makes a significant contribution in advancing and propagating knowledge in the field of cell and molecular biology. Cell Biology is a scientific discipline which involves study of the basic unit of life, cell. Research work under the domain revolves around the study of cell organelles, physiology, cell-cell interactions, molecular biochemistry, genetics, cell death and reproduction etc.
Cell Biology: Research & Therapy is a hybrid, peer reviewed, scholarly journal that provides a dual mode of publication; open access & subscription, thus facilitates wider reachability and visibility of the published work and a range of options to purchase our articles and also permits unlimited Internet Access to complete Journal content. It accepts research, review papers, online letters to the editors & brief comments on previously published articles or other relevant findings in SciTechnol. Articles submitted by authors are evaluated by a group of peer review experts in the field and ensures that the published articles are of high quality, reflect solid scholarship in their fields, and that the information they contain is accurate and reliable.
Scope and Relevance of the Journal:
Cell Signalling & Transduction
Stem Cell Biology: Research & Application
Application of Bioinformatics, Proteomics & Computational Biology in Cell Science
The journal uses Editorial Manager System for quality in review process. Editorial Manager is an online manuscript submission, review and tracking system. Review processing is performed by the editorial board members of Cell Biology: Research & Therapy journal or experts from outside. Minimum two independent reviewer’s approval followed by editor approval is required for acceptance of any citable manuscript. Authors may submit manuscripts and track their progress through the system. Reviewers can download manuscripts and submit their opinions to the editor whereas editors can manage the whole submission/review/revise/publish process via editorial manager.
Distribution of Characteristic Mutations in Native Ductal Adenocarcinoma of the Pancreas and Pancreatic Cancer Cell Lines
Although oncological treatment of pancreatic adenocarcinoma (PDAC) has improved within the last few years, PDAC continues to have a very low 5- year survival rate. Basic research is needed to improve and develop new therapeutic strategies. Pancreatic tumour cell lines (CLs) are a prerequisite for such basic research. However, the isolation of CLs is challenging. Outgrowth of cells is only achieved in a small proportion of tumour samples, although the reason for this poor growth remains unknown.
Chemotherapy Increases Aggressiveness of Prostate Cancer via Epithelial Mesenchymal Transition
Although chemotherapy has been used as a major therapeutic weapon against advanced prostate cancer, overcoming drug resistance is still a major challenge. Cancer has been known to diminish therapeutic effect by several molecular mechanisms– increasing efflux by recruiting cell membrane pumps and limiting drug diffusion by constructing leaky vasculature. Moreover, recent studies suggest that long-term treatment with chemotherapy may have detrimental effects for patients presenting with solid tumors. Specifically, prostate cancer epithelial cells develop resistance to chemotherapy and may convert into mesenchymal cells. This switching process, known as Epithelial to Mesenchymal Transition (EMT), is a critical precursor in prostate cancer invasion and metastasis.
NGF and APP Interplay: Focus on YENPTY Motif of Amyloid Precursor Protein and Y682 Residue
Cholinergic deficits originated from NGF metabolism disruption, represent one of the early changes in Alzheimer’s disease, where abnormal deposition of β-amyloid peptide (Aβ) and phosphorylated Tau define the neuropathological hallmarks of the disorder. A failure in NGF maturation can promote pro-apoptotic pathway activation, through p75 receptor; while lack of NGF signalling can generate an atypical TrkA receptor phosphorylation resulting in neuronal cell death and Aβ toxicity. These evidences suggest a complex interaction between TrkA, p75, and Aβ, whose exact cellular mechanisms remain still elusive. Here, we provide a general overview on the current knowledge on NGF and APP interplay, focusing on the events that mediate NGF signalling impairment, and, mostly, on the role of APP Tyrosine 682 phosphorylation whose absence in APPY682G mice impairs APP/TrkA interaction and leads to cholinergicneurodegeneration.
The human skeletal system is a dynamic system that plays vital roles in the sustenance of life. Bone loss is a phenomenon that occurs in humans both in short and in long term spaceflights. The phenotype can be also reproduced on the ground in human and animals and also modeled in cell-based analogs. With limited missions in space, experimental studies in these analogs have provided much of our understanding of bone loss.