UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. ソラレン・紫外線A（PUVA）光化学療法 psoralen plus ultraviolet a puva photochemotherapy
2. ビタミンAの概要 overview of vitamin a
3. 褥瘡の予防 prevention of pressure ulcers
4. 遺伝性の魚鱗癬の概要 overview of the inherited ichthyoses
5. 滴状乾癬 guttate psoriasis

English Journal

The Role of LAT-PLCγ1 Interaction in γδ T Cell Development and Homeostasis.

Sullivan SA, Zhu M, Bao S, Lewis CA, Ou-Yang CW, Zhang W.Author information Department of Immunology, Duke University Medical Center, Durham, NC 27710.AbstractLAT is a transmembrane adaptor protein that is vital for integrating TCR-mediated signals to modulate T cell development, activation, and proliferation. Upon T cell activation, LAT is phosphorylated and associates with Grb2, Gads, and PLCγ1 through its four distal tyrosine residues. Mutation of one of these tyrosines, Y136, abolishes LAT binding to PLCγ1. This results in impaired TCR-mediated calcium mobilization and Erk activation. CD4 αβ T cells in LATY136F knock-in mice undergo uncontrolled expansion, resulting in a severe autoimmune syndrome. In this study, we investigated the importance of the LAT-PLCγ1 interaction in γδ T cells by crossing LATY136F mice with TCRβ-/- mice. Our data showed that the LATY136F mutation had no major effect on homeostasis of epithelial γδ T cells, which could be found in the skin and small intestine. Interestingly, a population of CD4+ γδ T cells in the spleen and lymph nodes underwent continuous expansion and produced elevated amounts of IL-4, resulting in an autoimmune syndrome similar to that caused by αβ T cells in LATY136F mice. Development of these hyperproliferative γδ T cells was not dependent on MHC class II expression or CD4, and their proliferation could be suppressed, in part, by regulatory T cells. Our data indicated that a unique subset of CD4 γδ T cells can hyperproliferate in LATY136F mice and suggested that LAT-PLCγ1 signaling may function differently in various subsets of γδ T cells.
Journal of immunology (Baltimore, Md. : 1950).J Immunol.2014 Feb 12. [Epub ahead of print]
LAT is a transmembrane adaptor protein that is vital for integrating TCR-mediated signals to modulate T cell development, activation, and proliferation. Upon T cell activation, LAT is phosphorylated and associates with Grb2, Gads, and PLCγ1 through its four distal tyrosine residues. Mutation of one
PMID 24523509

Importance of Sphingosine Kinase (SphK) as a Target in Developing Cancer Therapeutics and Recent Developments in the Synthesis of Novel SphK Inhibitors.

Plano D, Amin S, Sharma AK.Author information Department of Pharmacology, Penn State Hershey Cancer Institute, CH72, Penn State College of Medicine , 500 University Drive, Hershey, Pennsylvania 17033, United States.AbstractSphingosine kinase (SphK) is an oncogenic lipid kinase that regulates the sphingolipid metabolic pathway that has been shown to play a role in numerous hyperproliferative/inflammatory diseases. The SphK isoforms (SphK1 and SphK2) catalyze the conversion of the proapoptotic substrate d-erythrosphingosine to the promitogenic/migratory product sphingosine 1-phosphate (S1P). Accumulation of S1P has been linked to the development/progression of cancer and various other diseases including, but not limited to, asthma, inflammatory bowel disease, rheumatoid arthritis, and diabetic nephropathy. SphK therefore represents a potential new target for developing novel therapeutics for cancer and other diseases. This finding has stimulated the development and evaluation of numerous SphK inhibitors over the past decade or so. In this review, we highlight the recent advancement in the field of SphK inhibitors including SphK1 and SphK2 specific inhibitors. Both sphingolipid based and nolipidic small molecule inhibitors and their importance in treatment of cancer and other diseases are discussed.
Journal of medicinal chemistry.J Med Chem.2014 Feb 11. [Epub ahead of print]
Sphingosine kinase (SphK) is an oncogenic lipid kinase that regulates the sphingolipid metabolic pathway that has been shown to play a role in numerous hyperproliferative/inflammatory diseases. The SphK isoforms (SphK1 and SphK2) catalyze the conversion of the proapoptotic substrate d-erythrosphingo
PMID 24471412

The Ah receptor in stem cell cycling, regulation, and quiescence.

Gasiewicz TA, Singh KP, Bennett JA.Author information Department of Environmental Medicine, University of Rochester Medical Center, Rochester, New York.AbstractProcesses that regulate quiescence, self-renewal, and differentiation of hematopoietic stem cells (HSCs) are not well understood. Owing, in part, to the ability of xenobiotic ligands to have persistent effects on the immune system in experimental animals, there has been much work to define a physiological role of the aryl hydrocarbon receptor (AhR) and its relationship to human disease. Persistent AhR activation by dioxin, a potent agonist, results in altered numbers and function of HSCs in mice. HSCs from AhR-/- knockout (KO) mice are hyperproliferative and have an altered cell cycle. Aging KO mice show characteristics consistent with premature bone marrow exhaustion. We propose that the increased proliferation of HSCs lacking AhR expression or activity is a result of loss of quiescence, and as such, AhR normally acts as a negative regulator to curb excessive or unnecessary proliferation. Similarly, prolonged and/or inappropriate stimulation of AhR activity may compromise the ability of HSCs to sense environmental signals that allow these cells to balance quiescence, proliferation, migration, and differentiation. These data and others support a hypothesis that deregulation of AhR function has an important role in HSC regulation and in the etiology and/or progression of certain hematopoietic diseases, many of which are associated with aging.
Annals of the New York Academy of Sciences.Ann N Y Acad Sci.2014 Feb 3. doi: 10.1111/nyas.12361. [Epub ahead of print]
Processes that regulate quiescence, self-renewal, and differentiation of hematopoietic stem cells (HSCs) are not well understood. Owing, in part, to the ability of xenobiotic ligands to have persistent effects on the immune system in experimental animals, there has been much work to define a physiol
PMID 24495120

Japanese Journal

B_1 and B_2 kinin receptor participation in hyperproliferative and inflammatory skin processes in mice

PIETROVSKI Evelise Fernandes,PALUDO Katia Sabrina,MENDES Daniel Augusto Gasparin Bueno,DE SOUZA FONSECA GUIMARAES Fernando,SANCHEZ VEIGA Silvio,DE FREITAS BUCHI Dorly,FONSECA Raphael Gomes,ZAMPRONIO Aleksander Roberto,BADER Michael,PESQUERO Joao Bosco,FERREIRA Juliano,OTUKI Michel Fleith,CABRINI Daniela Almeida
Journal of dermatological science 64(1), 23-30, 2011-10-01
NAID 10030892789

Cyclin D1/cdk4, estrogen receptors α and β, in N-methyl-N'-nitro-N-nitrosoguanidine-induced rat gastric carcinogenesis : immunohistochemical study

Motohashi Masaya,Wakui Shin,Muto Tomoko [他],SUZUKI Yoshihiko,SHIRAI Masaru,TAKAHASHI Hiroyuki,HANO Hiroshi
Journal of toxicological sciences 36(3), 373-378, 2011-06-01
… Hyperproliferative cell growth due to cyclin D1/cdk4, marker of cellular proliferation, is considered to be regulated by the expression of estrogen receptors (ERs). …
NAID 10029136038

ビタミンDの代謝および生理活性発現機構の解明と栄養疫学研究

岡野登志夫
ビタミン 83(1), 1-8, 2009-01-25
… 1α,25-Dihydroxyvitamin D_3 [1,25(OH)_2D_3] has been shown to modulate not only proliferation and differentiation but also apoptosis of malignant cells, indicating that it would be useful for the treatment of hyperproliferative diseases such as cancer and psoriasis. …
NAID 110007046148

Related Pictures

So, have a look at the slide. Look to see Related Hyperproliferative Disorders Buch Hyperproliferative and inflammatory Chronic benign hyperproliferative disease cells contribute to the hyperproliferative Next figure | Previous figure | Figure and hyperproliferative scar ” is a chronic hyperproliferative