Protein kinase C (PKC), which is involved in cell signaling pathways, comprises a family of serine/threonine kinases ubiquitously present in animals and its members are grouped on the basis of structural and activation characteristics into novel, classical, and atypical PKC forms. In this study, an atypical PKC of Macrobrachium rosenbergii, designated MraPKC, was successfully cloned, and its protein comprised structural domains similar to those of atypical PKC homologues, including the Phox and Bem1 (PB1) domain, a zinc finger phorbol-ester/DAG-type signature, protein kinase signatures, and a cAMP-dependent, cGMP-dependent, and PKC (AGC) kinase C-terminal domain. Phylogenetic analyses revealed a close evolutionary relationship between MraPKC and aPKCs of insects. MraPKC transcripts were detected in all tissues examined through an RT-PCR, with the highest level detected in muscles. A quantitative real-time PCR was used to evaluate MraPKC expression in hemocytes of M. rosenbergii in various molt stages, and in prawn challenged with Vibrio alginolyticus, Lactococcus garvieae, and white spot syndrome virus (WSSV) as well as in prawns injected with pathogen-associated molecular patterns (PAMPs), including lipopolysaccharide (LPS), peptidoglycan (PG), and polyinosinic:polycytidylic acid (Poly:IC). Results revealed that the expression pattern of MraPKC was distinctly modulated during molting, with significant enhancement in the C stage. MraPKC transcripts significantly increased in hemocytes of prawns infected with L. garvieae at 6-24 h and those injected with PG at 12-24 h. In contrast, significantly decreased expression of MraPKC was observed in hemocytes of prawns injected with V. alginolyticus and LPS for 3 and 12 h, respectively, and a similar phenomenon was observed in hemocytes of those injected with WSSV and Poly:IC for 12 h each. Therefore, MraPKC might play crucial roles in biological processes, and it may mediate the signaling pathway induced by varied pathogens for the potential regulation of host innate defense.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.fsi.2017.08.014DOI Listing

Publication Analysis

Top Keywords

protein kinase
12
atypical pkc
12
macrobrachium rosenbergii
8
mrapkc
8
mrapkc transcripts
8
prawns injected
8
hemocytes prawns
8
observed hemocytes
8
hemocytes
5
pkc
5

Similar Publications

Drug Development.

Alzheimers Dement

December 2024

Biosplice Therapeutics, Inc., San Diego, CA, USA.

Background: DYRK1A overexpression, common in neurodegenerative diseases like Alzheimer's (AD), contributes to neurofibrillary tangles via Tau protein hyperphosphorylation and amyloid plaque formation, key AD hallmarks. Therefore, DYRK1A has been regarded as a novel target for neurodegenerative diseases. However, developing DYRK1A selective inhibitors has been a difficult challenge due to the highly conserved ATP-binding site of protein kinases, particularly among the CMGC family.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Yonsei University, Incheon, Incheon, Korea, Republic of (South).

Background: Cyclin Y (CCNY) is a member of cyclin protein family inhibiting long-term synaptic plasticity, which is related to the learning and memory function in neuronal system. Recently, CCNY has been reported to associate with the cognitive deficits in Alzheimer's disease (AD).

Method: In this study, we discovered PFTAIRE peptide to diminish CCNY protein level and to ameliorate cognitive dysfunction in AD.

View Article and Find Full Text PDF

Background: Focusing on novel AD treatments, the TREAT-AD centers offer an array of free research tools, shared via the AD Knowledge Portal in a Target Enablement Package (TEP). This abstract showcases the research conducted by the IUSM-Purdue TREAT-AD Center, specifically focusing on Targeting class-II PI3K's as a potential breakthrough in AD therapy. Endocytosis within the brain encompasses diverse pathways for internalizing extracellular cargoes and receptors into cells.

View Article and Find Full Text PDF

Background: SHIP1 is a phosphatidyl inositol phosphatase encoded by INPP5D, which has been identified as a risk gene for Alzheimer's disease (AD). SHIP1 is expressed in microglia, the resident macrophage in brain. It is a complex, multidomain protein that acts as a negative regulator downstream from TREM2.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Department of Neurology, University of Fukui, Matsuoka, Fukui, Japan.

Background: One of the pathological hallmarks in Alzheimer's disease (AD) brain is neurofibrillary tangles (NFTs) composed of highly phosphorylated tau protein. Clinical benefit of traditional Japanese Kampo Yokukansan for dementia patients, including AD was suggested. In this study, we investigated whether yokukansan participates in the degradation of phosphorylated tau and toxic oligomeric species of tau by using cell culture model of tauopathy, M1C cells.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!