Using stakeholder insights to enhance engagement in PhD professional development.

There is increasing awareness of the need for pre- and post-doctoral professional development and career guidance, however many academic institutions are only beginning to build out these functional roles. As a graduate career educator, accessing vast silos and resources at a university and with industry-partners can be daunting, yet collaboration and network development are crucial to the success of any career and professional development office. To better inform and direct these efforts, forty-five stakeholders external and internal to academic institutions were identified and interviewed to gather perspectives on topics critical to career development offices.

Applying Experiential Learning to Career Development Training for Biomedical Graduate Students and Postdocs: Perspectives on Program Development and Design.

Experiential learning is an effective educational tool across many academic disciplines, including career development. Nine different institutions bridged by the National Institutes of Health Broadening Experiences in Scientific Training Consortium compared their experiments in rethinking and expanding training of predoctoral graduate students and postdoctoral scholars in the biomedical sciences to include experiential learning opportunities. In this article, we provide an overview of the four types of experiential learning approaches our institutions offer and compare the learning objectives and evaluation strategies employed for each type.

Retinoic acid induces expression of SLP-76: expression with c-FMS enhances ERK activation and retinoic acid-induced differentiation/G0 arrest of HL-60 cells.

Retinoic acid (RA) is known to cause MAPK signaling which propels G0 arrest and myeloid differentiation of HL-60 human myeloblastic leukemia cells. The present studies show that RA up-regulated expression of SLP-76 (Src-homology 2 domain-containing leukocyte-specific phospho-protein of 76 kDa), which became a prominent tyrosine-phosphorylated protein in RA-treated cells. SLP-76 is a known adaptor molecule associated with T-cell receptor and MAPK signaling.

Retinoic acid-induced CD38 expression in HL-60 myeloblastic leukemia cells regulates cell differentiation or viability depending on expression levels.

Retinoic acid-induced expression of the CD38 ectoenzyme receptor in HL-60 human myeloblastic leukemia cells is regulated by RARalpha and RXR, and enhanced or prevented cell differentiation depending on the level of expression per cell. RARalpha activation caused CD38 expression, as did RXR activation but not as effectively. Inhibition of MAPK signaling through MEK inhibition diminished the induced expression by both RARs and RXRs.

retinoic acid, bromodeoxyuridine, and the Delta 205 mutant polyoma virus middle T antigen regulate expression levels of a common ensemble of proteins associated with early stages of inducing HL-60 leukemic cell differentiation.

Retinoic acid (RA), bromodeoxyuridine (BrdU), and the Delta 205 mutant polyoma middle T antigen affect the expression of a common ensemble of proteins in HL-60 human myeloblastic leukemia cells. Each of these agents is known to be able to prime HL-60 cells and accelerate subsequently induced myeloid or monocytic differentiation and G0 cell cycle arrest, suggesting that they have equal or identical cellular targets relevant to the early stages of inducing cell differentiation and G0 arrest. As a test of this possibility, a survey of protein expression changes induced by RA, BrdU, or Delta 205 transfection was performed.

A retinoic acid receptor beta/gamma-selective prodrug (tazarotene) plus a retinoid X receptor ligand induces extracellular signal-regulated kinase activation, retinoblastoma hypophosphorylation, G0 arrest, and cell differentiation.

Retinoic acid receptor (RAR)beta is perceived to function as a tumor suppressor gene in various contexts where its absence is associated with tumorigenicity and its presence causes cell cycle arrest. Tazarotene is a prodrug selective for RARbeta/gamma, thereby motivating interest in determining whether tazarotene might activate putative tumor suppressor activity. Using HL-60 human myeloblastic leukemia cells, a cell line that undergoes G0 cell cycle arrest and myeloid differentiation in response to retinoic acid (RA), tazarotene failed to cause extracellular signal-regulated kinase (ERK) activation, a requirement for retinoic acid (RA)-induced G0 arrest and differentiation; retinoblastoma (RB) hypophosphorylation, another characteristic of RA-induced G0 arrest and cell differentiation; G0 arrest; or differentiation into mature myeloid cells.

Retinoic acid, bromodeoxyuridine, and the Δ205 mutant polyoma virus middle T antigen regulate expression levels of a common ensemble of proteins associated with early stages of inducing HL-60 leukemic cell differentiation.

Retinoic acid (RA), bromodeoxyuridine (BrdU), and the Δ205 mutant polyoma middle T antigen affect the expression of a common ensemble of proteins in HL-60 human myeloblastic leukemia cells. Each of these agents is known to be able to prime HL-60 cells and accelerate subsequently induced myeloid or monocytic differentiation and G0 cell cycle arrest, suggesting that they have equal or identical cellular targets relevent to the early stages of inducing cell differentiation and G0 arrest. As a test of this possibility, a survey of protein expression changes induced by RA, BrdU, or Δ205 transfection was performed.

Retinoic acid-induced growth arrest and differentiation: retinoic acid up-regulates CD32 (Fc gammaRII) expression, the ectopic expression of which retards the cell cycle.

Retinoic acid is known to cause the cell cycle arrest and myeloid differentiation of HL-60 myeloblastic leukemia cells. Evidence suggesting the possible involvement of the Fc gammaRII immunoglobulin receptor in mediating retinoic acid-induced growth arrest and differentiation of HL-60 cells is presented. HL-60 cells stably transfected with the delta205 mutant polyoma middle T antigen, a largely debilitated polyoma middle T antigen, are known to undergo accelerated retinoic acid-induced growth arrest and differentiation compared with parental HL-60 cells.