This is Actual scientists labelling Actual enzymes and I could not make this up if I tried. This is a cascade reaction from some extra-cellular signal.

Mitogen-Acitivated-Protein-Kinase-Kinase-Kinase

is activating

Mitogen-Activated-Protein-Kinase-Kinase

is activating

Mitogen-Activated-Protein-Kinase.

These are the real names.

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The cardinal lesion of diabetic nephropathy resides in renal glomeruli and is called diabetic glomerulosclerosis, hyperglycemia is responsible for the development and progression of diabetic nephropathy through metabolic derangements, including increased oxidative stress, renal polyol formation, activation of protein kinase C (PKC) mitogen activated protein kinases (MAPKs), and accumulation of advanced glycation end products, as well as such hemodynamic factors as systemic hypertension and increased intraglomerular pressure

7

Nadie puede imaginar como comienza…
Algún día la vi y me pareció bonita, de cierto modo
me identifique con ella.
Un día me entere que estaría conviviendo con ella
al menos 2 años.
Nuestros gustos e ideas eran similares, por lo que nos hicimos
compañeras.
La miraba 8 horas, 5 veces  a la semana.
Tal vez ahí.. empezó nuestra historia.
16 años, pretendíamos comernos el mundo.
Respetaba mis ideas, como yo las suyas.
Siempre fue mas madura y desde el inicio,
su hombro siempre estuvo disponible para
una niña inmadura y sensible.
Ella decía lo que mis oídos querían escuchar,
sus palabras eran plena sabiduría.
Escucho las buenas y las malas noticias,
mis mejores y los peores días estuvo conmigo.
No recuerdo cuando fue la primera vez
que le llame “mejor amiga” , en realidad no
importa tanto recordarlo, ambas tenemos
recuerdos de la adolescencia que guardamos
en la memoria.
BEST F R I E N D S NEVER END

PETITION FOR CHINESE RIGHTS

https://petitions.whitehouse.gov/petition/%E6%8A%97%E8%AE%AE%E4%B8%AD%E5%9B%BD%E6%B2%A1%E6%9C%89%E4%BA%BA%E6%9D%83%EF%BC%81%E6%8A%97%E8%AE%AE%E4%B8%AD%E5%9B%BD%E5%8F%B8%E6%B3%95%E4%B8%8D%E5%85%AC%EF%BC%81%E6%8A%97%E8%AE%AE%E4%B8%AD%E5%9B%BD%E8%B4%AA%E6%B1%A1%E8%85%90%E8%B4%A5%EF%BC%81-please-do-not-delete-petition-%E8%AF%B7%E4%B8%8D%E8%A6%81%E5%88%A0%E9%99%A4%E8%BF%99%E4%B8%AA%E8%AF%B7%E6%84%BF/DGwpB8M1

PKM2 gene regulates the behavior of pancreatic cancer cells via mitogen-activated protein kinase pathways.

PKM2 gene regulates the behavior of pancreatic cancer cells via mitogen-activated protein kinase pathways.

Mol Med Rep. 2014 Nov 20;

Authors: Feng J, Ma T, Ge Z, Lin J, Ding W, Chen H, Zhu W, Zhou S, Tan Y

Abstract
The aim of the current study was to investigate the effect of the PKM2 gene on the proliferation, invasion, migration and apoptosis of Panc‑1 and Sw1990 pancreatic cancer cells via its interaction with the mitogen‑activated protein kinases (MAPKs) signaling pathways. The expression levels of PKM2 protein in pancreatic cancer cells and the corresponding normal tissues was determined with western blot analysis. Immunohistochemical analysis of PKM2 expression was carried out in paraffin‑embedded sections of pancreatic cancer tissue. Two human pancreatic cancer cell lines were cultured in vitro, and a small interfering RNA (siRNA) was designed for the PKM2 gene and transfected into the cells. Cell proliferation was measured via an MTT assay, cell migration and invasion was measured via Transwell® chambers, and the effect of PKM2 on apoptosis was detected from B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein expression levels. Protein expression levels of the MAPK pathway proteins extracellular signal‑regulated kinase 1/2 (ERK1/2), p38 and c‑Jun N‑terminal kinase (JNK) and their phosphorylated forms were measured via western blot analysis. The expression level of PKM2 was significantly upregulated in the pancreatic cancer tissue compared with that of the corresponding normal tissue. Downregulation of PKM2 expression reduced the proliferation, migration and invasion of pancreatic cancer cell lines, while increasing the levels of apoptosis. Additionally, the expression levels of the phosphorylated‑(p‑)ERK1/2 and p‑p38 of the MAPK pathway in the PKM2 siRNA groups were markedly downregulated compared with those of the controls; however, the expression levels of ERK1/2, p38, JNK, p‑p38 and p‑JNK had no significantly changes compared with those of the control groups. In summary, the PKM2 gene has an important role in the proliferation, invasion, migration and apoptosis of Panc‑1 and Sw1990 pancreatic cancer cells, which may be associated with the expression of ERK1/2 and p38 of the MAPK signaling cascade.

PMID: 25411978 [PubMed - as supplied by publisher]



via pubmed: lymphoma daily http://ift.tt/1uiioQ2

Exposure to short-term air pollution components thus resulted in quantifiable epigenetic changes in the promoter areas of MAPK pathway genes. Bioinformatic mapping of single- vs. multi-exposure-associated epigenetic changes suggests that these alterations might affect biological pathways in nuanced ways that are not simply additive or fully predictable via individual-level exposure assessments.

EGCG could be used in the prevention or in the therapy of anthrax infections.

PMID:  EMBO Rep. 2004 Apr ;5(4):418-22. Epub 2004 Mar 12. PMID: 15031715 Abstract Title:  Potent inhibitors of anthrax lethal factor from green tea. Abstract:  The anthrax lethal factor (LF) has a major role in the development of anthrax. LF is delivered by the protective antigen (PA) inside the cell, where it exerts its metalloprotease activity on the N-terminus of MAPK-kinases. PA+LF are cytotoxic to macrophages in culture and kill the Fischer 344 rat when injected intravenously. We describe here the properties of some polyphenols contained in green tea as powerful inhibitors of LF metalloproteolytic activity, and how the main catechin of green tea, (-)epigallocatechin-3-gallate, prevents the LF-induced death of macrophages and Fischer 344 rats. http://j.mp/11hibFN

The combination of bortezomib with enzastaurin or lenalidomide enhances cytotoxicity in follicular and mantle cell lymphoma cell lines.

The combination of bortezomib with enzastaurin or lenalidomide enhances cytotoxicity in follicular and mantle cell lymphoma cell lines.

Hematol Oncol. 2014 Nov 13;

Authors: Cosenza M, Civallero M, Pozzi S, Marcheselli L, Bari A, Sacchi S

Abstract
We analyzed the combination of a proteasome inhibitor (bortezomib) with enzastaurin (PKC/AKT-inhibitor) or lenalidomide (immunomodulatory agent) for the inhibition of proliferation and induction of apoptosis in B-cell lymphoma cell lines and primary malignant cells. The effects of bortezomib, enzastaurin or lenalidomide, alone or in combinations, on cell viability and apoptosis were evaluated using the Cell Proliferation Kit and flow cytometry analysis. The interaction between drugs was examined by the Chou-Talalay method. Cell cycle analysis was performed by flow cytometry. The PI3K/AKT, PKC and MAPK/ERK signaling pathways were analyzed using western blot. Bortezomib with either enzastaurin or lenalidomide synergistically induced anti-proliferative and pro-apoptotic effects in B-cell lymphoma cells, even in the presence of the bone marrow microenvironment. The direct cytotoxicity is mediated by signaling events involving the PI3K/AKT, PKC and MAPK/ERK pathways leading to cell death. The significant increase of apoptosis was mediated by an increased ratio of pro-apoptotic proteins (Bax, Bad and Bim) to anti-apoptotic proteins (Bcl-2, Bcl-xL and Mcl-1), triggering the cleavage of caspases -3, -9, -8 and PARP. Further evaluation of the combination of bortezomib with enzastaurin or lenalidomide for the treatment of B-cell lymphoma is warranted, with the goal to improve the quality of life and survival of patients. Copyright © 2014 John Wiley & Sons, Ltd.

PMID: 25394177 [PubMed - as supplied by publisher]



via pubmed: lymphoma daily http://ift.tt/1u9fLmV
Rutin decreases lipopolysaccharide-induced acute lung injury via inhibition of oxidative stress and the MAPK-NF-κB pathway.

PubMed:


Related Articles

Rutin decreases lipopolysaccharide-induced acute lung injury via inhibition of oxidative stress and the MAPK-NF-κB pathway.

Free Radic Biol Med. 2014 Apr;69:249-57 

Authors: Yeh CH, Yang JJ, Yang ML, Li YC, Kuan YH

Abstract
Acute lung injury (ALI) is a serious disease with unacceptably high mortality and morbidity rates. Up to now, no effective therapeutic strategy for ALI has been established. Rutin, quercetin-3-rhamnosyl glucoside, expresses a wide range of biological activities and pharmacological effects, such as anti-inflammatory, antihypertensive, anticarcinogenic, vasoprotective, and cardioprotective activities. Pretreatment with rutin inhibited not only histopathological changes in lung tissues but also infiltration of polymorphonuclear granulocytes into bronchoalveolar lavage fluid in lipopolysaccharide (LPS)-induced ALI. In addition, LPS-induced inflammatory responses, including increased secretion of proinflammatory cytokines and lipid peroxidation, were inhibited by rutin in a concentration-dependent manner. Furthermore, rutin suppressed phosphorylation of NF-κB and MAPK and degradation of IκB, an NF-κB inhibitor. Decreased activities of antioxidative enzymes such as superoxide dismutase, catalase, glutathione peroxidase, and heme oxygenase-1 caused by LPS were reversed by rutin. At the same time, we found that ALI amelioration by chelation of extracellular metal ions with rutin is more efficacious than with deferoxamine. These results indicate that the protective mechanism of rutin is through inhibition of MAPK-NF-κB activation and upregulation of antioxidative enzymes.

PMID: 24486341 [PubMed - indexed for MEDLINE] http://dlvr.it/7SpDqC