Psychotherapy with Alexithymic Patients

Krystal, Henry

doi:10.1007/978-1-4684-4496-4_75

Cited by 15 publications

(21 citation statements)

References 2 publications

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“…Furthermore, in SI Fig. 9A, similar ChIP experiments were performed by using erythroid cells isolated from the spleen of phenylhydrazine-treated mice (36). Erythroid (Ter119ϩ) cells were first enriched by depleting all other cell types with a mix of lineage markers.…”

Section: Mediator Subunit Med1 Is Required For Transcriptional Activamentioning

confidence: 99%

The mediator complex functions as a coactivator for GATA-1 in erythropoiesis via subunit Med1/TRAP220

Stumpf

Waskow

Krötschel

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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The Mediator complex forms the bridge between transcriptional activators and RNA polymerase II. Mediator subunit Med1/TRAP220 is a key component of Mediator originally found to associate with nuclear hormone receptors. Med1 deficiency causes lethality at embryonic day 11.5 because of defects in heart and placenta development. Here we show that Med1-deficient 10.5 days postcoitum embryos are anemic but have normal numbers of hematopoietic progenitor cells. Med1-deficient progenitor cells have a defect in forming erythroid burst-forming units (BFU-E) and colony-forming units (CFU-E), but not in forming myeloid colonies. At the molecular level, we demonstrate that Med1 interacts physically with the erythroid master regulator GATA-1. In transcription assays, Med1 deficiency leads to a defect in GATA-1-mediated transactivation. In chromatin immunoprecipitation experiments, we find Mediator components at GATA-1-occupied enhancer sites. Thus, we conclude that Mediator subunit Med1 acts as a pivotal coactivator for GATA-1 in erythroid development.

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Section: Mediator Subunit Med1 Is Required For Transcriptional Activamentioning

confidence: 99%

The mediator complex functions as a coactivator for GATA-1 in erythropoiesis via subunit Med1/TRAP220

Stumpf

Waskow

Krötschel

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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“…Mice were sacrificed on day 5 by cervical dislocation, the spleen was removed, and a single cell suspension was prepared (25,26). To isolate erythroid lineage cells (27), the spleen cell suspension was washed and labeled with Ter-119 Microbeads (10 l/1 ϫ 10 7 cells; Miltenyi Biotech, Auburn, CA).…”

Section: Methodsmentioning

confidence: 99%

Erythropoietin Modulates Calcium Influx through TRPC2

Chu¹,

Cheung

Barber

et al. 2002

Journal of Biological Chemistry

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“…Viability was determined by eosin dye exclusion (Tilbrook et al, 1996b) and hemoglobin synthesis by benzidine staining (Klinken et al, 1988;Busfield and Klinken, 1992). Proliferation was assayed by [ 3 H]thymidine incorporation as described previously (Busfield and Klinken, 1992) using a modification of the method established by Krystal (1983).…”

Section: Cell Culturementioning

confidence: 99%

Lyn deficiency reduces GATA-1, EKLF and STAT5, and induces extramedullary stress erythropoiesis

et al. 2004

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In vitro studies have implicated the Lyn tyrosine kinase in erythropoietin signaling. In this study, we show that J2E erythroid cells lacking Lyn have impaired signaling and reduced levels of transcription factors STAT5a, EKLF and GATA-1. Since mice lacking STAT5, EKLF or GATA-1 have red cell abnormalities, this study also examined the erythroid compartment of Lyn À/À mice. Significantly, STAT5, EKLF and GATA-1 levels were appreciably lower in Lyn À/À erythroblasts, and the phenotype of Lyn À/À animals was remarkably similar to GATA-1 low animals. Although young adult Lyn-deficient mice had normal hematocrits, older mice developed anemia. Grossly enlarged erythroblasts and florid erythrophagocytosis were detected in the bone marrow of mice lacking Lyn. Markedly elevated erythroid progenitors and precursor levels were observed in the spleens, but not bone marrow, of Lyn À/À animals indicating that extramedullary erythropoiesis was occurring. These data indicate that Lyn À/À mice display extramedullary stress erythropoiesis to compensate for intrinsic and extrinsic erythroid defects.

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Psychotherapy with Alexithymic Patients

Cited by 15 publications

References 2 publications

The mediator complex functions as a coactivator for GATA-1 in erythropoiesis via subunit Med1/TRAP220

The mediator complex functions as a coactivator for GATA-1 in erythropoiesis via subunit Med1/TRAP220

Erythropoietin Modulates Calcium Influx through TRPC2

Lyn deficiency reduces GATA-1, EKLF and STAT5, and induces extramedullary stress erythropoiesis

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