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Signaling mechanisms and neutrophil ...
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Lin, Phoebe.
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Signaling mechanisms and neutrophil modulation through the lysophosphatidylcholine receptor, G2A.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Signaling mechanisms and neutrophil modulation through the lysophosphatidylcholine receptor, G2A./
作者:
Lin, Phoebe.
面頁冊數:
137 p.
附註:
Adviser: Richard D. Ye.
Contained By:
Dissertation Abstracts International67-05B.
標題:
Health Sciences, Immunology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3218785
ISBN:
9780542701498
Signaling mechanisms and neutrophil modulation through the lysophosphatidylcholine receptor, G2A.
Lin, Phoebe.
Signaling mechanisms and neutrophil modulation through the lysophosphatidylcholine receptor, G2A.
- 137 p.
Adviser: Richard D. Ye.
Thesis (Ph.D.)--University of Illinois at Chicago, Health Sciences Center, 2006.
G2A is a lysophospholipid receptor found only in tissues of hematopoietic origin. Its G protein coupling profile and effects on neutrophil function were examined in detail.
ISBN: 9780542701498Subjects--Topical Terms:
1017716
Health Sciences, Immunology.
Signaling mechanisms and neutrophil modulation through the lysophosphatidylcholine receptor, G2A.
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Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2494.
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Thesis (Ph.D.)--University of Illinois at Chicago, Health Sciences Center, 2006.
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G2A is a lysophospholipid receptor found only in tissues of hematopoietic origin. Its G protein coupling profile and effects on neutrophil function were examined in detail.
520
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It was found that G2A couples constitutively to Galphas, Galphaq, and Galpha13. Its endogenously produced lipid ligand, lysophosphatidylcholine (LPC), also stimulated the Gas pathway resulting in a further elevation of cyclic adenosine monophosphate (CAMP). The phenotypic effect of this combination of G proteins activated by this receptor culminates in apoptosis of G2A-expressing cells, including a transfected cell line, and lymphocytes, which express G2A endogenously.
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LPC stimulation of neutrophils, which also express G2A endogenously, had an inhibitory effect. LPC inhibited neutrophil superoxide generation, chemotaxis, degranulation, and neutrophil-mediated tissue damage as shown in an ex vivo mouse lung model of tissue reperfusion injury. This cumulative effect suggests that LPC, perhaps through its action on the receptor, G2A, plays a regulatory role in the control of neutrophil function.
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