scholarly journals Evasion of Host Defence by Leishmania donovani: Subversion of Signaling Pathways

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Md. Shadab ◽  
Nahid Ali
Keyword(s):  
Signaling Pathways ◽  
Leishmania Donovani ◽  
Severe Infection ◽  
Skin Lesions ◽  
Host Cells ◽  
Self Healing ◽  
Protozoan Parasites ◽  
Kinase C ◽  
Map Kinase Pathway ◽  
Kinase Pathway

Protozoan parasites of the genus Leishmania are responsible for causing a variety of human diseases known as leishmaniasis, which range from self-healing skin lesions to severe infection of visceral organs that are often fatal if left untreated. Leishmania donovani (L. donovani), the causative agent of visceral leishmaniasis, exemplifys a devious organism that has developed the ability to invade and replicate within host macrophage. In fact, the parasite has evolved strategies to interfere with a broad range of signaling processes in macrophage that includes Protein Kinase C, the JAK2/STAT1 cascade, and the MAP Kinase pathway. This paper focuses on how L. donovani modulates these signaling pathways that favour its survival and persistence in host cells.

scholarly journals Signaling pathways in cerebral vasospasm

2011 ◽  
Vol 30 (03) ◽  
pp. 116-119
Author(s):  
Flávio Ramalho Romero ◽  
Eberval Gadelha Figueiredo ◽  
Manoel Jacobsen Teixeira
Keyword(s):  
Signaling Pathways ◽  
Cerebral Vasospasm ◽  
Vascular Remodeling ◽  
Myosin Light Chain ◽  
Experimental Treatment ◽  
Kinase C ◽  
New Development ◽  
Map Kinase Pathway ◽  
Multiple Signaling ◽  
Kinase Pathway

AbstractCerebral vasospasm is a deadly complication following the rupture of intracranial aneurysms. One new development in the experimental treatment of cerebral vasospasm is the looming target of signaling pathways. The pathogenesis of cerebral vasospasm involves multiple signaling pathways in proliferation, inflammation, cell death, smooth muscle phenotype changes, vascular remodeling, and contraction. A review of all of these areas is beyond the scope of this article, and as such, three systems that mediate these vascular responses have been selected: the tyrosine kinase-MAP kinase pathway, the sphingosine-1-Rho myosin light chain kinase pathway and protein kinase C.

B3 10:45 Activation of the RAS-RAF-MAP kinase pathway in red drum leukocytes by a staurosporine-insensitive protein kinase C

1997 ◽  
Vol 21 (2) ◽  
pp. 94
Author(s):  
Patricia A. Mericko ◽  
Kent C. MacDougal ◽  
Kathryn E. Meier ◽  
Karen G. Burnett ◽  
Grice Marine
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Map Kinase ◽  
Red Drum ◽  
Kinase C ◽  
Map Kinase Pathway ◽  
Kinase Pathway

scholarly journals PV1 Is a Key Structural Component for the Formation of the Stomatal and Fenestral Diaphragms

2004 ◽  
Vol 15 (8) ◽  
pp. 3615-3630 ◽  
Author(s):  
Radu V. Stan ◽  
Eugene Tkachenko ◽  
Ingrid R. Niesman
Keyword(s):  
Endothelial Cells ◽  
Structural Component ◽  
De Novo ◽  
Cell Types ◽  
Microvascular Endothelial Cells ◽  
Myristate Acetate ◽  
Kinase C ◽  
Map Kinase Pathway ◽  
Kinase Pathway

PV1 is an endothelial-specific integral membrane glycoprotein associated with the stomatal diaphragms of caveolae, transendothelial channels, and vesiculo-vacuolar organelles and the diaphragms of endothelial fenestrae. Multiple PV1 homodimers are found within each stomatal and fenestral diaphragm. We investigated the function of PV1 within these diaphragms and their regulation and found that treatment of endothelial cells in culture with phorbol myristate acetate (PMA) led to upregulation of PV1. This correlated with de novo formation of stomatal diaphragms of caveolae and transendothelial channels as well as fenestrae upon PMA treatment. The newly formed diaphragms could be labeled with anti-PV1 antibodies. The upregulation of PV1 and formation of stomatal and fenestral diaphragms by PMA was endothelium specific and was the highest in microvascular endothelial cells compared with their large vessel counterparts. By using a siRNA approach, PV1 mRNA silencing prevented the de novo formation of the diaphragms of caveolae as well as fenestrae and transendothelial channels. Overexpression of PV1 in endothelial cells as well as in cell types that do not harbor caveolar diaphragms in situ induced de novo formation of caveolar stomatal diaphragms. Lastly, PV1 upregulation by PMA required the activation of Erk1/2 MAP kinase pathway and was protein kinase C independent. Taken together, these data show that PV1 is a key structural component, necessary for the biogenesis of the stomatal and fenestral diaphragms.

scholarly journals Central Asian Rodents as Model Animals for Leishmania major and Leishmania donovani Research

2020 ◽  
Vol 8 (9) ◽  
pp. 1440
Author(s):  
Barbora Vojtkova ◽  
Tatiana Spitzova ◽  
Jan Votypka ◽  
Tereza Lestinova ◽  
Iveta Kominkova ◽  
...  
Keyword(s):  
Standard Model ◽  
Leishmania Donovani ◽  
Leishmania Major ◽  
Skin Lesions ◽  
Rodent Species ◽  
Sand Fly ◽  
Phodopus Sungorus ◽  
Self Healing ◽  
Natural Sand ◽  
Disease Spectrum

The clinical manifestation of leishmaniases depends on parasite species, host genetic background, and immune response. Manifestations of human leishmaniases are highly variable, ranging from self-healing skin lesions to fatal visceral disease. The scope of standard model hosts is insufficient to mimic well the wide disease spectrum, which compels the introduction of new model animals for leishmaniasis research. In this article, we study the susceptibility of three Asian rodent species (Cricetulus griseus, Lagurus lagurus, and Phodopus sungorus) to Leishmania major and L. donovani. The external manifestation of the disease, distribution, as well as load of parasites and infectiousness to natural sand fly vectors, were compared with standard models, BALB/c mice and Mesocricetus auratus. No significant differences were found in disease outcomes in animals inoculated with sand fly- or culture-derived parasites. All Asian rodent species were highly susceptible to L. major. Phodopus sungorus showed the non-healing phenotype with the progressive growth of ulcerative lesions and massive parasite loads. Lagurus lagurus and C. griseus represented the healing phenotype, the latter with high infectiousness to vectors, mimicking best the character of natural reservoir hosts. Both, L. lagurus and C. griseus were also highly susceptible to L. donovani, having wider parasite distribution and higher parasite loads and infectiousness than standard model animals.

Alteration of Bcl11b upon stimulation of both the MAP kinase- and Gsk3-dependent signaling pathways in double-negative thymocytes

2019 ◽  
Vol 97 (2) ◽  
pp. 201-213 ◽  
Author(s):  
Wisam Hussein Selman ◽  
Elahe Esfandiari ◽  
Theresa M. Filtz
Keyword(s):  
Map Kinase ◽  
Signaling Pathways ◽  
Developmental Stages ◽  
B Cell Lymphoma ◽  
Double Negative ◽  
Thymocyte Development ◽  
Double Positive ◽  
Map Kinase Pathway ◽  
Kinase Pathway ◽  
Stimulation Of

B-cell lymphoma/leukemia 11B (Bcl11b) is a transcription factor critical for thymocyte development. We have previously characterized the kinetic post-translational modifications (PTMs) of Bcl11b in double-positive (DP) thymocytes during stimulation of the T cell receptor-activated MAP kinase pathway. However, the PTMs of Bcl11b in thymocytes from other developmental stages in the thymus, primarily double-negative (DN) cells, have not been previously identified. We found that kinetic modifications of Bcl11b in DN cells are somewhat different than the patterns observed in DP cells. Distinct from DP thymocytes, phosphorylation and sumoylation of Bcl11b in DN cells were not oppositely regulated in response to activation of MAP kinase, even though hyper-phosphorylation of Bcl11b coincided with near complete desumoylation. Additionally, prolonged stimulation of the MAP kinase pathway in DN cells, unlike DP thymocytes, did not alter Bcl11b levels of sumoylation or ubiquitinylation, or stability. On the other hand, activation of Wnt–Gsk3-dependent signaling in DN cells resulted in composite dephosphorylation and sumoylation of Bcl11b. Moreover, stimulation of MAP kinase and (or) Wnt signaling pathways differentially affects gene expression of some Bcl11b target and maturation-associated genes. Defining the signaling pathways and regulation of sequence-specific transcription factors by PTMs at various stages of thymopoiesis may improve our understanding of leukemogenesis.

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