In naive T cells, Lck exerts a negative control on the ERK/MAPK pathway. We show that c-mip (c-maf inducing protein) interacts with the p85 subunit of PI3 kinase and inactivates Lck, which results in Erk1/2 and p38 MAPK activation. This effect is not enough to activate AP1 given the inability of ERK to migrate into the nucleus and to transactivate its target genes. We demonstrate that c-mip interacts with Dip1 and upregulates DAPK, which blocks the nuclear translocation of ERK1/2. This dual effect of c-mip is unique and might represent a potential mechanism to prevent the development of an immune response.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.febslet.2009.12.015 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Biomarkers for diagnosis of stage III, grade C with molar incisor pattern periodontitis in children and young adults: a systematic review and meta-analysis.
Clin Oral Investig
September 2023
Centre for Host Microbiome Interactions, Faculty of Dentistry, Oral and Craniofacial Sciences, King's College London, London, UK.
Aim: To explore the existing salivary, gingival crevicular fluid (GCF), blood, and serum biomarkers associated with grade C molar-incisor pattern (C/MIP) periodontitis in systemically healthy children and young adults.
Materials And Methods: Cross-sectional, case-control, and cohort studies on stage III grade C periodontitis or former equivalent diagnosis with analysis of molecular biomarkers in saliva, GCF, blood, or serum were retrieved from six databases and screened based on the eligibility criteria. The risk of bias in included studies was evaluated.
Molecular and Cellular Mechanisms for Proteinuria in Minimal Change Disease.
Front Med (Lausanne)
June 2018
Laboratory of Molecular Nephrology, Genoa, Italy.
Minimal Change Disease (MCD) is a clinical condition characterized by acute nephrotic syndrome, no evident renal lesions at histology and good response to steroids. However, frequent recurrence of the disease requires additional therapies associated with steroids. Such multi-drug dependence and frequent relapses may cause disease evolution to focal and segmental glomerulosclerosis (FSGS) over time.
View Article and Find Full Text PDFInhibition of nephrin activation by c-mip through Csk-Cbp-Fyn axis plays a critical role in Angiotensin II-induced podocyte damage.
Cell Signal
March 2013
Department of Nephrology, First People's Hospital of Kunshan, the Affiliated Kunshan Hospital of Jiangsu University, Jiangsu,215300, China.
It has been demonstrated that nephrin inactivation plays a critical role in Angiotensin II (AngII)-induced podocyte damage both in in vitro and in vivo, but the underlying molecular mechanisms are still unclear. Recently, c-maf inducing protein (c-mip) has been identified as a key component in the molecular pathogenesis of acquired podocyte diseases. In this study, the role of c-mip on AngII-induced nephrin inactivation and podocyte damage was explored in a mouse podocyte cell line.
View Article and Find Full Text PDFGroup-selective enrichment and determination of pyrethroid insecticides in aquaculture seawater via molecularly imprinted solid phase extraction coupled with gas chromatography-electron capture detection.
J Chromatogr A
March 2012
Key Laboratory of Applied Technology of Marine Biology, Ministry of Education, Ningbo University, 818 Fenghua Road, Ningbo 315211, China.
Two types of molecularly imprinted polymers (MIPs) for the simultaneous determination of six pyrethroid insecticides have been developed using deltamethrin (D-MIPs) and cypermethrin (C-MIPs) as template molecules. A comparison of the performance of D-MIPs, C-MIPs, and the corresponding non-imprinted polymers (NIPs) were conducted. Stronger group-selective interactions between the C-MIPs and the six pyrethroid insecticides were achieved.
View Article and Find Full Text PDFc-mip impairs podocyte proximal signaling and induces heavy proteinuria.
Sci Signal
May 2010
INSERM, UMR 955, Equipe 21, F-94010 Créteil, France.
Idiopathic nephrotic syndrome comprises several podocyte diseases of unknown origin that affect the glomerular podocyte, which controls the permeability of the filtration barrier in the kidney to proteins. It is characterized by the daily loss of more than 3 g of protein in urine and the lack of inflammatory lesions or cell infiltration. We found that the abundance of c-mip (c-maf inducing protein) was increased in the podocytes of patients with various acquired idiopathic nephrotic syndromes in which the podocyte is the main target of injury.
View Article and Find Full Text PDFWant 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!