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.


is activating


is activating


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


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
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.


Structure of the BRAF-MEK Complex Reveals a Kinase Activity Independent Role for BRAF in MAPK Signaling

Publication date:
Source:Cancer Cell
Author(s): Jacob R. Haling , Jawahar Sudhamsu , Ivana Yen , Steve Sideris , Wendy Sandoval , Wilson Phung , Brandon J. Bravo , Anthony M. Giannetti , Ariana Peck , Alexandre Masselot , Tony Morales , Darin Smith , Barbara J. Brandhuber , Sarah G. Hymowitz , Shiva Malek

Graphical abstract


Cancer Cell
Emodin Inhibits Breast Cancer Cell Proliferation through the ERα-MAPK/Akt-Cyclin D1/Bcl-2 Signaling Pathway.

Emodin Inhibits Breast Cancer Cell Proliferation through the ERα-MAPK/Akt-Cyclin D1/Bcl-2 Signaling Pathway.

Asian Pac J Cancer Prev. 2014;15(15):6247-51

Authors: Sui JQ, Xie KP, Zou W, Xie MJ

BACKGROUND: The aim of the present study was to investigate the involvement of emodin on the growth of human breast cancer MCF-7 and MDA-MB-231 cells and the estrogen (E2) signal pathway in vitro.
MATERIALS AND METHODS: MTT assays were used to detect the effects of emodin on E2 induced proliferation of MCF-7 and MDA-MB-231 cells. Flow cytometry (FCM) was applied to determine the effect of emodin on E2-induced apoptosis of MCF-7 cells. Western blotting allowed detection of the effects of emodin on the expression of estrogen receptor α, cyclin D1 and B-cell lymphoma-2 (Bcl-2), mitogen-activated protein kinases (MAPK) and phosphatidylinostiol 3-kinases (PI3K). Luciferase assays were emplyed to assess transcriptional activity of ERα.
RESULTS: Emodin could inhibit E2-induced MCF-7 cell proliferation and anti-apoptosis effects, and arrest the cell cycle in G0/G1 phase, further blocking the effect of E2 on expression and transcriptional activity of ERα. Moreover, Emodin influenced the ER α genomic pathway via downregulation of cyclin D1 and Bcl-2 protein expression, and influenced the non-genomic pathway via decreased PI3K/Akt protein expression.
CONCLUSIONS: These findings indicate that emodin exerts inhibitory effects on MCF-7 cell proliferation via inhibiting both non-genomic and genomic pathways.

PMID: 25124606 [PubMed - in process]

via pubmed: lymphoma daily
Bilateral Subfoveal Neurosensory Retinal Detachment Associated With MEK Inhibitor Use for Metastatic Cancer

Three patients who received oral MEK inhibitors developed bilateral subfoveal neurosensory retinal detachment. Patient 1 had metastatic uveal melanoma; the findings resolved without intervention, and subsequent mild uveitis was responsive to topical corticosteroids. Patient 2 had metastatic cholangiocarcinoma, and his findings resolved after 2 weeks of observation. Patient 3 had metastatic rectal cancer, with bilateral uveitis and bilateral subfoveal retinal detachment. Her findings resolved with observation and topical corticosteroids for uveitis. No patient developed permanent ocular sequelae, and none withdrew from the clinical trial of MEK inhibitor therapy.
JAMA Ophthalmol. 2014;132(8):1005 doi:10.1001/jamaophthalmol.2014.976

A MEK inhibitor is a chemical or drug that inhibits the mitogen-activated protein kinase kinase enzymes MEK1 and/or MEK2. They can be used to affect the MAPK/ERK pathway which is often overactive in some cancers. (See MAPK/ERK pathway#Clinical significance.)

Hence MEK inhibitors have potential for treatment of some cancers,[1] especially BRAF-mutated melanoma,[2] and KRAS/BRAF mutated colorectal cancer.[3]

Some MEK inhibitors:

Trametinib (GSK1120212), FDA-approved to treat BRAF-mutated melanoma. Also studied in combination with BRAF inhibitor dabrafenib to treat BRAF-mutated melanoma.
Selumetinib, had a phase 2 clinical trial for non-small cell lung cancer (NSCLC) which demonstrated an improvement in PFS,[4] and is now in phase III development in KRAS mutation positive NSCLC (SELECT-1,NCT01933932). Other clinical trials underway include uveal melanoma, and differentiated thyroid carcinoma.

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Targeting the MAPK Pathway in GI Malignancies
EGCG and hesperetin may act as antiatherogenic agents blocking oxidized LDL-induced endothelial apoptosis.

PMID:  J Nutr. 2008 Jun ;138(6):983-90. PMID: 18492823 Abstract Title:  Dietary flavonoids differentially reduce oxidized LDL-induced apoptosis in human endothelial cells: role of MAPK- and JAK/STAT-signaling. Abstract:  Endothelial apoptosis is a driving force in atherosclerosis development. Oxidized LDL promotes inflammatory and thrombotic processes and is highly atherogenic, as it stimulates macrophage cholesterol accumulation and foam cell formation. This study investigated multiple mitogen-activated protein kinase (MAPK)-responsive death/survival signaling pathways, through which flavonoids of (-)epigallocatechin gallate (EGCG) and hesperetin exerted antiapoptosis in endothelial cells exposed to oxidized LDL. EGCG and hesperetin substantially diminished the oxidized LDL-induced 2’,7’-dichlorofluorecein staining, suggesting that these flavonoids inhibited intracellular accumulation of oxidized LDL-triggered reactive oxygen species and consequent apoptosis. The Western-blot data revealed that oxidized LDL upregulated c-Jun N-terminal kinase (JNK) phosphorylation, which was rapidly reversed by EGCG and hesperetin. They mitigated the consequent activation of the JNK downstream on p53 and c-Jun. Moreover, oxidized LDL increased luciferase activity of p53 in endothelial cells transfected with a p53 promoter construct, the increase of which was strikingly downregulated by EGCG and hesperetin. Surprisingly, hesperetin but not EGCG attenuated phosphorylation of p38MAPK and its downstream c-myc and signal transducers and activators of transcription (STAT)1 evoked by oxidized LDL. This study also attempted to explore a linkage of Janus kinase (JAK)2/STAT3 activation to MAPK signaling in oxidized LDL-induced endothelial apoptosis. Notably, we found that the JAK2 inhibitor substantially blocked the JNK activation. Our findings suggest that EGCG and hesperetin may act as antiatherogenic agents blocking oxidized LDL-induced endothelial apoptosis via differential cellular apoptotic machinery. These data provide evidence that the interplay between p38MAPK and JAK-STAT pathways is involved in dietary flavonoid protection against oxidized LDL through hampering MAPK-dependent pathways involving the activation of JAK2.