Extracellular Signal-Regulated MAP Kinases

Publication Title: 
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

Spinal muscular atrophy (SMA), a recessive neurodegenerative disease, is characterized by the selective loss of spinal motor neurons. No available therapy exists for SMA, which represents one of the leading genetic causes of death in childhood. SMA is caused by a mutation of the survival-of-motor-neuron 1 (SMN1) gene, leading to a quantitative defect in the survival-motor-neuron (SMN) protein expression. All patients retain one or more copies of the SMN2 gene, which modulates the disease severity by producing a small amount of stable SMN protein.

Author(s): 
Branchu, Julien
Biondi, Olivier
Chali, Farah
Collin, Thibault
Leroy, Felix
Mamchaoui, Kamel
Makoukji, Joelle
Pariset, Claude
Lopes, Philippe
Massaad, Charbel
Chanoine, Christophe
Charbonnier, FrÈdÈric
Publication Title: 
British Journal of Pharmacology

BACKGROUND AND PURPOSE: Artemisinin and its derivatives exhibit potent immunosuppressive activity. The purpose of the current study was to examine the immunosuppressive activity of artemether directly on T lymphocytes and to explore its potential mode of action. EXPERIMENTAL APPROACH: In vitro, T-cell proliferation was measured using [(3)H]-thymidine incorporation assay in cells stimulated with ConA, alloantigen and anti-CD3 antibody. CFSE-labeled cell division and cell cycle distribution were monitored by flow cytometry.

Author(s): 
Wang, J.-X.
Tang, W.
Shi, L.-P.
Wan, J.
Zhou, R.
Ni, J.
Fu, Y.-F.
Yang, Y.-F.
Li, Y.
Zuo, J.-P.
Publication Title: 
Cancer Research

Guggulsterone, a constituent of Indian Ayurvedic medicinal plant Commiphora mukul, causes apoptosis in cancer cells but the sequence of events leading to cell death is poorly understood. We now show that guggulsterone-induced cell death in human prostate cancer cells is caused by reactive oxygen intermediate (ROI)-dependent activation of c-Jun NH(2)-terminal kinase (JNK).

Author(s): 
Singh, Shivendra V.
Choi, Sunga
Zeng, Yan
Hahm, Eun-Ryeong
Xiao, Dong
Publication Title: 
BMC cancer

BACKGROUND: Triphala is commonly used in Ayurvedic medicine to treat variety of diseases; however its mechanism of action remains unexplored. This study elucidates the molecular mechanism of Triphala against human pancreatic cancer in the cellular and in vivo model. METHODS: Growth-inhibitory effects of Triphala were evaluated in Capan-2, BxPC-3 and HPDE-6 cells by Sulphoradamine-B assay. Apoptosis was determined by cell death assay and western blotting. Triphala was administered orally to nude mice implanted with Capan-2 xenograft.

Author(s): 
Shi, Yan
Sahu, Ravi P.
Srivastava, Sanjay K.
Publication Title: 
Cancer Research

Guggulsterone, a constituent of Indian Ayurvedic medicinal plant Commiphora mukul, causes apoptosis in cancer cells but the sequence of events leading to cell death is poorly understood. We now show that guggulsterone-induced cell death in human prostate cancer cells is caused by reactive oxygen intermediate (ROI)-dependent activation of c-Jun NH(2)-terminal kinase (JNK).

Author(s): 
Singh, Shivendra V.
Choi, Sunga
Zeng, Yan
Hahm, Eun-Ryeong
Xiao, Dong
Publication Title: 
BMC cancer

BACKGROUND: Triphala is commonly used in Ayurvedic medicine to treat variety of diseases; however its mechanism of action remains unexplored. This study elucidates the molecular mechanism of Triphala against human pancreatic cancer in the cellular and in vivo model. METHODS: Growth-inhibitory effects of Triphala were evaluated in Capan-2, BxPC-3 and HPDE-6 cells by Sulphoradamine-B assay. Apoptosis was determined by cell death assay and western blotting. Triphala was administered orally to nude mice implanted with Capan-2 xenograft.

Author(s): 
Shi, Yan
Sahu, Ravi P.
Srivastava, Sanjay K.
Publication Title: 
Canadian Journal of Physiology and Pharmacology

Ayurveda is an Indian system of medicine. Despite clinical efficacy, lack of scientific validation has limited the effective use of Ayurvedic drugs. Cardoguard is an Ayurvedic antihypertensive drug formulated by Nagarjuna Herbal Concentrates Ltd., Kerala, India. Left ventricular hypertrophy (LVH) is a modifiable risk factor, and regression of LVH reduces the propensity for adverse cardiovascular events. This study was taken up with the objective of evaluating the efficacy of Cardoguard in the prevention of cardiac remodeling.

Author(s): 
Sankar, Vandana
Nair, Renuka R.
Harikrishnan, Vijayakumar S.
Fernandez, Adelaide C.
Kumar, Cherumanal S. Krishna
Madhavachandran, Viswanathamenon
Publication Title: 
The Journal of Biological Chemistry

The roles of MEK, ERK, the epsilon and alpha isoforms of protein kinase C (PKC), and caveolin-1 in regulating collagen expression were studied in normal lung fibroblasts. Knocking down caveolin-1 gave particularly striking results. A 70% decrease caused a 5-fold increase in MEK/ERK activation and collagen expression. The combined data reveal a branched signaling pathway. In its central portion MEK activates ERK, leading to increased collagen expression. Two branches converge on MEK/ERK. In one, increased PKCepsilon leads to MEK/ERK activation.

Author(s): 
Tourkina, Elena
Gooz, Pal
Pannu, Jaspreet
Bonner, Michael
Scholz, Dimitri
Hacker, Sharon
Silver, Richard M.
Trojanowska, Maria
Hoffman, Stanley
Publication Title: 
Cardiovascular Research

OBJECTIVE: Resistin may be associated with obesity and cardiovascular diseases. However, it is unknown whether resistin directly contributes to angiogenesis. In the present study, we evaluated the effects of resistin on angiogenic potential, including endothelial cell proliferation, migration, and capillary-like tube formation. METHODS: Human coronary artery endothelial cells (HCAECs) were treated with resistin. Cell proliferation was evaluated by [3H]thymidine incorporation and MTS assays. Cell migration was assessed by a modified Boyden chamber assay.

Author(s): 
Mu, Hong
Ohashi, Ryuji
Yan, Shaoyu
Chai, Hong
Yang, Hui
Lin, Peter
Yao, Qizhi
Chen, Changyi
Publication Title: 
Brain Research

MAP kinase is associated with delta-opioid receptor (DOR) signaling and plays a role in cell survival/death. Since anisomycin may alter MAP kinase activity and affect neuronal survival, we investigated whether anisomycin alters neuronal response to hypoxic stress and DOR inhibition. The experiments were performed in cultured cortical neurons. MAP kinase activities were determined by immunoblotting and neuronal viability was assessed by LDH leakage and live/dead morphological study.

Author(s): 
Hong, Soon-Sun
Qian, Hong
Zhao, Peng
Bazzy-Asaad, Alia
Xia, Ying

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