Insulin stimulates Ca2+ uptake via PKC, cAMP, and p38 MAPK in mouse embryonic stem cells

Han, Ho Jae; Lee, Yun Jung

doi:10.1016/j.lfs.2004.10.060

Cited by 14 publications

(10 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The MAPK pathway is activated by many stimulatory agents and phosphorylates downstream signaling molecules (16). Insulin also activates MAPK (24,32,49), and MAPK activation leads to Hsp27 phosphorylation (1,25,35,39,63). Thus, in the present study, we used phosphospecific antibodies to detect phosphorylated isoforms of Hsp27.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Insulin-induced myocardial protection in isolated ischemic rat hearts requires p38 MAPK phosphorylation of Hsp27

Ali²,

Currie³

2008

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

“…Once insulin activates the insulin receptor, the PI3K/Akt and MAPK pathways are activated (55). Recent evidence indicates that insulin activates ERK1/2 and p38 MAPK (3,25,35,41). p38 MAPK, in turn, activates MAPKAPK-2 that directly regulates the phosphorylation of Hsp27 (1,39,69).…”

Section: Discussionmentioning

confidence: 99%

Insulin-induced myocardial protection in isolated ischemic rat hearts requires p38 MAPK phosphorylation of Hsp27

Ali²,

Currie³

2008

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…Genistein also acts as a PTK inhibitor through a variety of mechanisms, including competing with adenosine triphosphate (ATP) at the tyrosine kinase ATP-binding site of epidermal growth factor receptors [26,27], inhibiting c-src [28,29] (a PTK involved in mitogen-activated protein kinase (MAPK)] or activating p38 MAPK at the transforming growth factor-β receptor level [30]. Isoflavone-mediated inhibition of PTK has also been demonstrated in studies investigating tumor necrosis factor (TNF), Toll-like receptor and growth factor signaling cascades [18,31].…”

Section: General Mechanisms Of Action Of Isoflavonesmentioning

confidence: 99%

Soy isoflavones and virus infections

Andres

Donovan

Kuhlenschmidt

2009

The Journal of Nutritional Biochemistry

111

View full text Add to dashboard Cite

Isoflavones and their related flavonoid compounds exert antiviral properties in vitro and in vivo against a wide range of viruses. Genistein is, by far, the most studied soy isoflavone in this regard, and it has been shown to inhibit the infectivity of enveloped or nonenveloped viruses, as well as single-stranded or double-stranded RNA or DNA viruses. At concentrations ranging from physiological to supraphysiological (3.7-370 muM), flavonoids, including genistein, have been shown to reduce the infectivity of a variety of viruses affecting humans and animals, including adenovirus, herpes simplex virus, human immunodeficiency virus, porcine reproductive and respiratory syndrome virus, and rotavirus. Although the biological properties of the flavonoids are well studied, the mechanisms of action underlying their antiviral properties have not been fully elucidated. Current results suggest a combination of effects on both the virus and the host cell. Isoflavones have been reported to affect virus binding, entry, replication, viral protein translation and formation of certain virus envelope glycoprotein complexes. Isoflavones also affect a variety of host cell signaling processes, including induction of gene transcription factors and secretion of cytokines. The efficacy of isoflavones and related flavonoids in virus infectivity in in vitro bioassays is dependent on the dose, frequency of administration and combination of isoflavones used. Despite promising in vitro results, there is lack of data confirming the in vivo efficacy of soy isoflavones. Thus, investigations using appropriate in vivo virus infectivity models to examine pharmacological and especially physiological doses of flavonoids are warranted.

show abstract

“…These cells closely resemble their in vivo counterparts and provide a stable in vitro model of embryonic growth and development. In addition, they provide a tool whereby specific signaling systems can be investigated [15, 16]. Therefore, this study examined the effect of ATP on mouse ESC proliferation and its related signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

ATP Stimulates Mouse Embryonic Stem Cell Proliferation via Protein Kinase C, Phosphatidylinositol 3‐Kinase/Akt, and Mitogen‐Activated Protein Kinase Signaling Pathways

2006

Self Cite

View full text Add to dashboard Cite

show abstract

Insulin stimulates Ca2+ uptake via PKC, cAMP, and p38 MAPK in mouse embryonic stem cells

Cited by 14 publications

References 43 publications

Insulin-induced myocardial protection in isolated ischemic rat hearts requires p38 MAPK phosphorylation of Hsp27

Insulin-induced myocardial protection in isolated ischemic rat hearts requires p38 MAPK phosphorylation of Hsp27

Soy isoflavones and virus infections

ATP Stimulates Mouse Embryonic Stem Cell Proliferation via Protein Kinase C, Phosphatidylinositol 3‐Kinase/Akt, and Mitogen‐Activated Protein Kinase Signaling Pathways

Contact Info

Product

Resources

About