The determinants of monitoring costs in not-for-profit organizations

Pearson, Timothy; Brooks, Richard C.

doi:10.1108/jpbafm-10-04-1996-b002

Cited by 4 publications

(16 citation statements)

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“…They find that dependence on external resources including the Single Audit and debt are positively associated with audit fees. In the only study we are aware of which examines the determinants of nonprofit accounting and audit fees, Pearson et al (1998) report program ratio (i.e., the ratio of program expenses to total expenses) and executive compensation, commonly scrutinized nonprofit metrics, as determinants. Dhaliwal et al (2012) and Chen (2009) utilize resource dependence theory to explain relationships between a for-profit organization and its stakeholders.…”

Section: 11mentioning

confidence: 99%

“…4 The few extant nonprofit audit fee studies have been limited to smaller samples consisting almost entirely of large nonprofit organizations (Vermeer, Raghunandan, and Forgione 2009a;Beattie, Goodacre, Pratt, and Stevenson 2001). We use accounting fees reported on Form 990 5 as a proxy for monitoring costs, inclusive of audit fees (Tate 2007;Pearson, Brooks, and Neidermeyer 1998) 2 We define monitoring costs as accounting fees as reported in Form 990, which include audit fees and other fees paid to external accountants. We limit our sample to nonprofit organizations that are required to have an audit based on state-specific criteria, and for a subset of our sample, audit fees comprise approximately 90.8 percent of accounting fees.…”

Section: Introductionmentioning

confidence: 99%

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Large Sample Evidence of the Determinants of Nonprofit Monitoring Costs: A Resource Dependence Framework

Webb

Waymire

2016

Journal of Governmental &Amp; Nonprofit Accounting

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Despite the importance of audit and accounting services in nonprofit organizations, few studies have examined determinants of these monitoring costs in this setting. This study provides large sample evidence (n ¼ 32,283 nonprofit entity-years) that reliance on external resources in the form of government grants is associated with higher monitoring costs, and that this effect is increased for large nonprofit organizations. In contrast, reliance on direct contributions, which are more likely to comprise smaller amounts from a more diverse group of resource providers, is associated with lower monitoring costs. We also find that, for larger nonprofits, reliance on internal resources (e.g., investment income) is associated with lower monitoring costs. These results are consistent with the tenets of resource dependence theory, i.e., reliance on certain external support that is hard to replace results in increased monitoring costs, and reliance on internal resources can reduce monitoring costs. These results demonstrate the implications of resource dependence on monitoring and offer practical benefit from the predictive models.

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Section: 11mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Large Sample Evidence of the Determinants of Nonprofit Monitoring Costs: A Resource Dependence Framework

Webb

Waymire

2016

Journal of Governmental &Amp; Nonprofit Accounting

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“…MAPK phosphorylates a serine residue in the AF-1 domain of the ERs. This modification is necessary for ac-tivation by peptide growth factors [30,32,42,54]. Since simply putting a negative charge at the AF-1 associated serine 118 of ERα is not sufficient for ligand-independent activation [32], other sites of ERα or other factors may need to be modified as well.…”

Section: Signaling Pathwaysmentioning

confidence: 99%

“…Tissuespecific differences in the signaling circuitry may provide part of the explanation [see, e.g., refs. 30,56]. The direct phosphorylation of steroid receptors by some of these pathways is important.…”

Section: Signaling Pathwaysmentioning

confidence: 99%

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Molecular mechanisms of cross-talk between growth factors and nuclear receptor signaling

Picard

2003

Pure and Applied Chemistry

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Signaling pathways can be linear, but more complex patterns are common. Growth factors and many other extracellular signals cannot directly enter cells and transduce their information via membrane-bound receptors. In contrast, steroid receptors are members of the nuclear receptor superfamily and await their cognate hormones inside the cells. These two types of signaling pathways are extensively intertwined and cross-talk at many different levels. A wide range of extra-and intracellular signals, including a variety of growth factors, can activate the transcriptional activity of steroid receptors in the absence of their cognate hormones. Conversely, steroid receptors lead a double life. By coupling to signaling molecules that mediate signal transduction of extracellular factors, they can elicit very rapid nongenomic responses. The signaling pathways of steroid-independent activation of steroid receptors, on the one hand, and of nongenomic signaling by steroid receptors, on the other, display a remarkable reciprocal relationship suggesting that these two modes of signaling cross-talk may be two faces of the same coin. DEFINITION AND OVERVIEWExtracellular signals modify intracellular processes through cognate receptors that elicit a cascade of events. However, a linear view of signal transduction falls short of describing all effects. Instead, branching, feedback, integration, and networking are characteristics of most if not all signal transduction pathways. Signaling cross-talk refers to a situation where one signal affects the output of another, seemingly distinct, signal transduction pathway.There is signaling cross-talk at all levels of signaling, from affecting availability of the signal to modifying the regulation of expression of target genes. For example, at the level of an organism, steroid hormone concentrations are influenced by signals that affect the levels of their serum binding proteins. Signals can stimulate the biosynthesis of other signals and their receptors. In breast cancer cells, estrogen induces the expression of the progesterone receptor (PR) [1], the EGF receptor [2], and several members of the EGF ligand family [3,4]. With respect to a target cell, signaling cross-talk may take place in the extracellular space or within the cell, inside or outside the nucleus.In this review, I will focus on the molecular mechanisms by which a variety of extra-and intracellular signals can modulate the activities of steroid receptors, in particular the receptors for the sex steroids, that is, the estrogen receptors (ERs) α and β, PR, and the androgen receptor (AR). These are all members of the nuclear receptor superfamily. Moreover, I will discuss how the very same nuclear receptors appear to elicit very rapid nongenomic effects by feeding into other signaling pathways. There is mounting evidence that these two nuclear receptor activities may be two faces of the same coin

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SKF-82958 Is a Subtype-selective Estrogen Receptor-α (ERα) Agonist That Induces Functional Interactions between ERα and AP-1

Walters

Dutertre

Smith

2002

Journal of Biological Chemistry

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The transcriptional activity of estrogen receptors (ERs) can be regulated by ligands as well as agents such as dopamine, which stimulate intracellular signaling pathways able to communicate with these receptors. We examined the ability of SKF-82958 (SKF), a previously characterized full dopamine D1 receptor agonist, to stimulate the transcriptional activity of ER␣ and ER␤. Treatment of HeLa cells with SKF-82958 stimulated robust ER␣-dependent transcription from an estrogen-response element-E1b-CAT reporter in the absence of estrogen, and this was accompanied by increased receptor phosphorylation. However, induction of ER␤-directed gene expression under the same conditions was negligible. In our cell model, SKF treatment did not elevate cAMP levels nor enhance transcription from a cAMPresponse element-linked reporter. Control studies revealed that SKF-82958, but not dopamine, competes with 17␤-estradiol for binding to ER␣ or ER␤ with comparable relative binding affinities. Therefore, SKF-82958 is an ER␣-selective agonist. Transcriptional activation of ER␣ by SKF was more potent than expected from its relative binding activity, and further examination revealed that this synthetic compound induced expression of an AP-1 target gene in a tetradecanoylphorbol-13-acetate-response element (TRE)-dependent manner. A putative TRE site upstream of the estrogen-response element and the amino-terminal domain of the receptor contributed to, but were not required for, SKF-induced expression of an ER␣-dependent reporter gene. Overexpression of the AP-1 protein c-Jun, but not c-Fos, strongly enhanced SKF-induced ER␣ target gene expression but only when the TRE was present. These studies provide information on the ability of a ligand that weakly stimulates ER␣ to yield strong stimulation of ER␣-dependent gene expression through cross-talk with other intracellular signaling pathways producing a robust combinatorial response within the cell.The effects of estrogens are mediated by the products of two separate genes, one for estrogen receptor-␣ (ER␣) 1 and another for ER␤. Both are members of the nuclear receptor superfamily of ligand-activated transcription factors. The mechanisms by which ERs activate target gene expression in response to estrogen signaling have been the subject of intense investigation since their respective cDNAs were cloned (1, 2). Because of the relatively recent identification of ER␤, the bulk of our knowledge regarding the genomic effects of estrogens is derived from ER␣ studies. For instance, upon binding to 17␤-estradiol (E 2 ), ER␣ undergoes a series of biochemical alterations including increased phosphorylation and conformational changes as well as homodimerization and binding of the receptor to its target DNA sequence, the estrogen-response element (ERE; see Refs. 3-5). ER␤ also undergoes conformational changes in response to ligand binding (6, 7) and is phosphorylated in vivo (8). With respect to DNA binding, ER␤ binds to the same consensus ERE that ER␣ does, although the latter receptor has an ϳ4-fold ...

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The determinants of monitoring costs in not-for-profit organizations

Cited by 4 publications

References 8 publications

Large Sample Evidence of the Determinants of Nonprofit Monitoring Costs: A Resource Dependence Framework

Large Sample Evidence of the Determinants of Nonprofit Monitoring Costs: A Resource Dependence Framework

Molecular mechanisms of cross-talk between growth factors and nuclear receptor signaling

SKF-82958 Is a Subtype-selective Estrogen Receptor-α (ERα) Agonist That Induces Functional Interactions between ERα and AP-1

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