A Tax-Based Test of the Dividend Signaling Hypothesis

Signaling Endosome Hypothesis: A Cellular Mechanism …

Modeling the signaling endosome hypothesis: Why a …

In addition, many studies have confirmed thatoverexpression of EGFR or the aberrant activation of the EGFRsignaling pathways are responsible for Tam-resistance (,).Activated Gαs promotes the degradation of EGFR (,),which reduces the expression of EGFR and blocks the EGFR signalingpathways indirectly, and then inhibits cell growth. Thus,consistently overactive Gαs inhibits the proliferation of TAM-Rcells by promoting the degradation of EGFR. Combined with ourresults, we provide an explanation for the estrogen-like activityof low-dose Tam in TAM-R cells and why high-dose Tam inhibits TAM-Rcell proliferation (). InTAM-R cells, the sensitivity of ER to Tam decreases, and theexpression of GPR30 is upregulated (). Therefore, Tam at a low concentrationcan promote the proliferation of TAM-R cells by furtherupregulating the expression and activation of GPR30. However, inthis case, Gαs is consistently overactive when GPR30 binds tohigh-dose Tam, and then continuous activation of Gαs promotes thedegradation of EGFR, whose expression decreases quickly andobviously. The degradation of EGFR results in the arrest of theactivation of ERK1/2 and AKT directly, which has an inhibitoryeffect on the proliferation of TAM-R cells. When the inhibitoryeffect of overactive Gαs which induces EGFR degradation overridesthe stimulating effect on proliferation via GPR30, the growth ofTAM-R cells is blocked. This hypothesis will provide answers towhether the estrogen-like effect of low-dose Tam or Tam at a highconcentration inhibits the proliferation of TAM-R cells viasuppression of the activation of ERK1/2 and AKT.

Red and near infra-red signaling: Hypothesis and perspectives

What is signaling hypothesis | pavicaruparnipobodandeku

Many studies have shown that the compliance to Tamdosage has a close relationship with the survival rate of breastcancer patients (). According toour results, we hypothesized that patients with an irregularmedication schedule have a poor survival rate as the drugconcentration in blood fails to maintain a relatively high level,and a low dose of Tam may play an estrogen-like role in promotingtumor growth after patients acquire breast cancer with Tamresistance. Therefore, to ensure a safe dose range, a relativelyhigh level of Tam is better for the control of disease and delaysthe progression to Tam-resistant breast cancer. In order to confirmour data and hypothesis, and more importantly to provide a powerfulconclusion to the standardized use of Tam, a large-scaleepidemiological survey should be implemented to identify thedifferences in the survival rates and disease progression indifferent Tam concentration groups. If possible, the optimal dosageof Tam should be identified by further investigation as soon aspossible to delay the occurrence of the Tam resistance, even toovercome the Tam resistance.


In order to investigate whether high-dose andlow-dose Tam have differential effects on ERK1/2 and AKT signalingpathways in TAM-R cells, we analyzed the phosphorylation of ERK1/2and AKT induced following treatment with 15 μM Tam. The activationof ERK1/2 was markedly and sustainably suppressed under thiscondition, which was different compared to treatment with 1 μM Tamin TAM-R cells (). Inaddition, the phosphorylation of AKT was inhibited in TAM-R cellsfollowing treatment with 15 μM Tam for 10 min (); however, after exposure to 1 μMTam, the levels of p-AKT in the TAM-R cells barely changed(). These results suggestedthat downregulation of p-ERK1/2 and p-AKT was caused by high-doseTam to inhibit TAM-R cell proliferation. Taken together, adose-response effect of Tam was noted on TAM-R cell proliferationand different doses of Tam had differential effects on ERK1/2 andAKT signaling pathways in TAM-R cells; thus we hypothesized thatdifferent doses of Tam stimulate or inhibit TAM-R cell growth viadifferent signaling pathways.

Bla i på emneord "signaling hypothesis" - BIBSYS

We propose and implement a new test of the dividend signaling hypothesis that is designed to discriminate between dividend signaling and other theories that would account for the apparent existence of a dividend preference. Our test refines the use of data on stock price responses to dividend announcements. In particular, we study the effect of dividend taxation on the bang-for-the-buck, which we define as the share price response per dollar of dividends. Most dividend signaling models imply that an increase in dividend taxation should increase the bang-for-the-buck. In contrast, other dividend preference theories imply that an increase in dividend taxation should decrease the bang-for-the-buck. Since there have recently been considerable variation in the tax treatment of dividends, we are able to study dividend announcement effects under different tax regimes. Our central finding is that there is a strong positive relationship between dividend tax rates and the bang-for-the-buck. This result supports the dividend signaling hypothesis, and is consistent with alternatives. The paper also provides corroborating evidence based on the relationship between the bang-for-the-buck and bond ratings.

What Is The signaling Hypothesis As It Re..

Since mitochondrial dysfunction is a major source of oxidative stress in aged tissues, we asked whether the basal activities of stress response signaling pathway(s) are indicative of oxidative stress in aged tissues. To address this issue we asked whether: (a) aging affects the basal activity of the p38 MAPK stress signaling pathway; (b) the p38 MAPK pathway is activated by 3-nitropropionic acid (3-NPA), an inhibitor of complex II (succinic dehydrogenase) and generator of reactive oxygen species (ROS); (c) aging affects the response of the p38α signaling pathway to 3-NPA. Our studies have shown that the basal kinase activities of p38α, its upstream activator, MKK3, and its downstream substrate, ATF-2, are elevated in livers of aged C57BL/6 male mice and that these kinase activities, which are induced by 3-NPA in young livers, do not occur in aged livers. Furthermore, although aging does not affect their protein pool levels there are specific increases in phosphorylation of threonine residues in the p38α and ATF-2 catalytic sites that might account for the increased basal level kinase activities in the aged livers. Our studies suggest that failure to respond to 3-NPA may be a factor in the susceptibility of aged tissue to oxidative damage, and support our hypothesis that aged tissues (especially liver) develop a state of chronic stress even in the absence of a challenge.