RAD Managers: Strategic Coaching for Managers and Leaders

Objective: Managerial coaching is a nascent area of research; as such there are few models supported by independent inquiry endorsing their effectiveness in impacting employee outcomes. The purpose of the current investigation was to present a concise, practical model of managerial coaching (RAD: relationships, accountability, development) that can be used for teaching and evaluating coaching behaviors. The model was hypothesized to predict ratings of coaching effectiveness (CE), perceptions of supervisor support (PSS), occupational self-efficacy (OSE), and work engagement (WE). Further, each factor of the model was tested in a series of secondary hypotheses to determine which factors were the most influential in predicting each outcome. Method: Participants consisted of 1477 employees who reported to 439 managers enrolled in managerial coaching workshops belonging to a variety of organizations from over 30 countries. Each employee rated managers on their coaching behaviors, CE, and PSS. They also provided self-ratings about their OSE and WE. This cross-sectional data was used in a series of multi-model regressions using a compositional approach to centering, which allows analysis of individual (L1) and group effects (L2) in addition to cross-level interactions. Results: The RAD model predicted CE (βL1 = 0.66; βL2 = 0.83), PSS (βL1 = 0.42; βL2 = 0.43; βinteraction = -0.17), OSE (βL1 = 0.18; βL2 = 0.15), and WE (βL1 = 0.45; βL2 = 0.39) with all significance levels at p \u3c .001. The L1 effects support the use of coaching with each direct report; the L2 effects suggest that outcomes show additional improvements when managers coach all their employees rather than just some. The cross-level interaction for PSS indicates that when managers coach all their employees, it can act as a buffer effect for employee perceptions even when managers do not do supportive behaviors for an individual employee. Secondary hypotheses revealed that each factor had differing individual- and group-level effects, suggesting that each factor could be used strategically to intentionally improve the different outcomes. Conclusions: This study adds to the mounting evidence for the potential effectiveness of managerial coaching across a variety of outcomes. The examination of each factor as a separate predictor provided insights about how managers might leverage strategic coaching, indicating that further research on multi-factored models may consider a similar nested design and statistical approach. Ultimately, the RAD model shows great promise for organizations interested in developing leaders and improving outcomes for employees

On structural accounts of model-explanations

The focus in the literature on scientific explanation has shifted in recent years towards model-based approaches. In recent work, Alisa Bokulich has argued that idealization has a central role to play in explanation. Bokulich claims that certain highly-idealized, structural models can be explanatory, even though they are not considered explanatory by causal, mechanistic, or covering law accounts of explanation. This paper focuses on Bokulich’s account in order to make the more general claim that there are problems with maintaining that a structural criterion can capture the way that highly-idealized models explain. This paper examines Bokulich’s claim that the structural model explanation of quantum wavefunction scarring, featuring semiclassical mechanics, is deeper than the explanation provided by the local quantum model. The challenge for Bokulich is to show that the semiclassical model answers a wider range of w-questions, as this is her method of assessing structural information. I look at two reasonable approaches employing w-questions, and I argue that neither approach is ultimately satisfactory. Because structural similarity has preferences for more fundamental models, I argue that the local quantum model provides explanations that at least as deep as the semiclassical ones. The criterion either wrongly identifies all models as explanatory, or prefers models from fundamental theory. Either way, it cannot capture the way that highly-idealized models explain

The relationship between insulin binding, insulin activation of insulin-receptor tyrosine kinase, and insulin stimulation of glucose uptake in isolated rat adipocytes

We have studied the relationship between insulin activation of insulin-receptor kinase and insulin stimulation of glucose uptake in isolated rat adipocytes. Glucose uptake was half-maximally or maximally stimulated, respectively, when only 4% or 14% of the maximal kinase activity had been reached. To investigate this relationship also under conditions where the insulin effect on activation of receptor kinase was decreased, the adipocytes were exposed to 10 microM-isoprenaline alone or with 5 micrograms of adenosine deaminase/ml. An approx. 30% (isoprenaline) or approx. 50% (isoprenaline + adenosine deaminase) decrease in the insulin effect on receptor kinase activity was found at insulin concentrations between 0.4 and 20 ng/ml, and this could not be explained by decreased insulin binding. The decreased insulin-effect on kinase activity was closely correlated with a loss of insulin-sensitivity of glucose uptake. Moreover, our data indicate that the relation between receptor kinase activity and glucose uptake (expressed as percentage of maximal uptake) remained unchanged. The following conclusions were drawn. (1) If activation of receptor kinase stimulates glucose uptake, only 14% of the maximal kinase activity is sufficient for maximal stimulation. (2) Isoprenaline decreases the coupling efficiency between insulin binding and receptor-kinase activation, this being accompanied by a corresponding decrease in sensitivity of glucose uptake. (3) Our data indicate that the signalling for glucose uptake is closely related to receptor-kinase activity, even when the coupling efficiency between insulin binding and kinase activation is altered. They thus support the hypothesis that receptor-kinase activity reflects the signal which originates from the receptor and which is transduced to the glucose-transport system

Purification and characterization of a protein-tyrosine kinase encoded by the Abelson murine leukemia virus

Sequences termed v-abl, which encode the protein-tyrosine kinase activity of Abelson murine leukemia virus, have been expressed in Escherichia coli as a fusion product (ptabl50 kinase). This fusion protein contains 80 amino acids of SV40 small t and the 403 amino acid protein kinase domain of v-abl. We report here the purification and characterization of this kinase. The purified material contains two proteins (Mr = 59,800 and 57,200), both of which possess sequences derived from v-abl. Overall purification was 3,750-fold, with a 31% yield, such that 117 micrograms of kinase could be obtained from 40 g of E. coli within 6-7 days. The specific kinase activity is over 170 mumol of phosphate min-1 mumol-1, comparable to the most active protein- serine kinases. Kinase activity is insensitive to K+, Na+, Ca2+, Ca2+- calmodulin, cAMP, or cAMP-dependent protein kinase inhibitor. The Km for ATP is dependent on the concentration of the second substrate. GTP can also be used as a phosphate donor. The enzyme can phosphorylate peptides consisting of as few as two amino acids and, at a very low rate, free tyrosine. Incubation of the kinase with [gamma-32P]ATP results in incorporation of 1.0 mol of phosphate/mol of protein. This reaction, however, cannot be blocked by prior incubation with unlabeled ATP. Incubation of 32P-labeled kinase with either ADP or ATP results in the synthesis of [32P]ATP. This suggests the phosphotyrosine residue on the Abelson kinase contains a high energy phosphate bond

Autophosphorylation at serine 166 regulates RIP kinase 1-mediated cell death and inflammation

Receptor interacting protein kinase 1 (RIPK1) regulates cell death and inflammatory responses downstream of TNFR1 and other receptors, and has been implicated in the pathogenesis of inflammatory and degenerative diseases. RIPK1 kinase activity induces apoptosis and necroptosis, however the mechanisms and phosphorylation events regulating RIPK1-dependent cell death signaling remain poorly understood. Here we show that RIPK1 autophosphorylation at serine 166 plays a critical role for the activation of RIPK1 kinase-dependent apoptosis and necroptosis. Moreover, we show that S166 phosphorylation is required for RIPK1 kinase-dependent pathogenesis of inflammatory pathologies in vivo in four relevant mouse models. Mechanistically, we provide evidence that trans autophosphorylation at S166 modulates RIPK1 kinase activation but is not by itself sufficient to induce cell death. These results show that S166 autophosphorylation licenses RIPK1 kinase activity to induce downstream cell death signaling and inflammation, suggesting that S166 phosphorylation can serve as a reliable biomarker for RIPK1 kinase-dependent pathologies

Localization of tyrosine kinase-coding region in v-abl oncogene by the expression of v-abl-encoded proteins in bacteria

A series of plasmids containing different segments of the v-abl oncogene have been constructed to express different portions of the v- abl protein in bacteria. The tyrosine kinase activity of these proteins was determined by an in vitro assay employing histones or angiotensin II as substrates for the v-abl-encoded tyrosine kinase. These experiments show that the 5'-1.2 kilobases of v-abl is necessary and sufficient to produce an active tyrosine kinase which is functional as a monomeric soluble protein. The kinase-coding region corresponds to the minimal region of v-abl required for the transformation of fibroblasts. The kinase-coding region also coincides with the conserved protein sequences which are found in other tyrosine kinases. A compact domain of the v-abl protein including this kinase-coding region can accumulate to high levels in bacteria. The C-terminal region of the v- abl protein is not needed for the kinase activity and is rapidly degraded in bacteria

Aldosterone signaling through transient receptor potential melastatin 7 cation channel (TRPM7) and its α-kinase domain

We demonstrated a role for the Mg2 + transporter TRPM7, a bifunctional protein with channel and α-kinase domains, in aldosterone signaling. Molecular mechanisms underlying this are elusive. Here we investigated the function of TRPM7 and its α-kinase domain on Mg2 + and pro-inflammatory signaling by aldosterone. Kidney cells (HEK-293) expressing wild-type human TRPM7 (WThTRPM7) or constructs in which the α-kinase domain was deleted (ΔKinase) or rendered inactive with a point mutation in the ATP binding site of the α-kinase domain (K1648R) were studied. Aldosterone rapidly increased [Mg2 +]i and stimulated NADPH oxidase-derived generation of reactive oxygen species (ROS) in WT hTRPM7 and TRPM7 kinase dead mutant cells. Translocation of annexin-1 and calpain-II and spectrin cleavage (calpain target) were increased by aldosterone in WT hTRPM7 cells but not in α-kinase-deficient cells. Aldosterone stimulated phosphorylation of MAP kinases and increased expression of pro-inflammatory mediators ICAM-1, Cox-2 and PAI-1 in Δkinase and K1648R cells, effects that were inhibited by eplerenone (mineralocorticoid receptor (MR) blocker). 2-APB, a TRPM7 channel inhibitor, abrogated aldosterone-induced Mg2 + responses in WT hTRPM7 and mutant cells. In 2-APB-treated ΔKinase and K1648R cells, aldosterone-stimulated inflammatory responses were unchanged. These data indicate that aldosterone stimulates Mg2 + influx and ROS production in a TRPM7-sensitive, kinase-insensitive manner, whereas activation of annexin-1 requires the TRPM7 kinase domain. Moreover TRPM7 α-kinase modulates inflammatory signaling by aldosterone in a TRPM7 channel/Mg2 +-independent manner. Our findings identify novel mechanisms for non-genomic actions of aldosterone involving differential signaling through MR-activated TRPM7 channel and α-kinase