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The Role of Phospholipid Scramblase ...

Chen, Chun-Wei David.

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The Role of Phospholipid Scramblase 1 in G-CSF-induced Granulopoiesis.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The Role of Phospholipid Scramblase 1 in G-CSF-induced Granulopoiesis./
作者:	Chen, Chun-Wei David.
面頁冊數:	164 p.
附註:	Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
Contained By:	Dissertation Abstracts International72-08B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3458554
ISBN:	9781124659145

The Role of Phospholipid Scramblase 1 in G-CSF-induced Granulopoiesis.
Chen, Chun-Wei David.

The Role of Phospholipid Scramblase 1 in G-CSF-induced Granulopoiesis. - 164 p.

Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .

Thesis (Ph.D.)--University of Rochester, 2011.

Phospholipid scramblase 1 (PLSCR1) was originally identified as an endofacial plasma membrane protein that mediates calcium-dependent bidirectional movement of phospholipids. Subsequent studies revealed that PLSCR1 also participates in kinase signaling pathways initiated through ligand-activated cell surface receptors such as the EGF and IgE receptors. In addition to its well recognized functions at the plasma membrane, PLSCR1 is capable of trafficking into the nucleus, resulting in transcriptional activation of its target genes including IP3R1. Accumulated evidence suggests that PLSCR1 participates in diverse biological events regulating cellular proliferation, differentiation, activation and apoptosis.

ISBN: 9781124659145Subjects--Topical Terms:

1017686
Biology, Cell.

The Role of Phospholipid Scramblase 1 in G-CSF-induced Granulopoiesis.
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245 1 4 $a The Role of Phospholipid Scramblase 1 in G-CSF-induced Granulopoiesis.
300 $a 164 p.
500 $a Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
500 $a Advisers: Peter J. Sims; Therese Wiedmer.
502 $a Thesis (Ph.D.)--University of Rochester, 2011.
520 $a Phospholipid scramblase 1 (PLSCR1) was originally identified as an endofacial plasma membrane protein that mediates calcium-dependent bidirectional movement of phospholipids. Subsequent studies revealed that PLSCR1 also participates in kinase signaling pathways initiated through ligand-activated cell surface receptors such as the EGF and IgE receptors. In addition to its well recognized functions at the plasma membrane, PLSCR1 is capable of trafficking into the nucleus, resulting in transcriptional activation of its target genes including IP3R1. Accumulated evidence suggests that PLSCR1 participates in diverse biological events regulating cellular proliferation, differentiation, activation and apoptosis.
520 $a More recently, a role for PLSCR1 in the innate immunity has been discovered. Mice deficient in PLSCR1 exhibit normal steady-state hematologic parameters but impaired "emergency granulopoiesis," a rapid, temporary increase in the number of circulating neutrophils that can be observed upon in vivo administration of granulocyte colony-stimulating factor (G-CSF). Nevertheless, the mechanism by which PLSCR1 contributes to the response of hematopoietic progenitors to G-CSF is largely unknown.
520 $a In this thesis we examined the contribution of PLSCR1 to G-CSF-induced emergency granulopoiesis using in vivo (mice), ex vivo (primary bone marrow cells) and in vitro (SCF-ER-Hoxb8 conditionally immortalized myeloid progenitors) experimental models. Our results suggest that PLSCR1 prolongs the period of mitotic expansion of granulocyte precursors under G-CSF, thereby giving rise to an increased number of neutrophils derived from their progenitors. This effect of PLSCR1 is not affected by mutation that prevents the membrane association of PLSCR1. By contrast, it is blocked by mutation in its nuclear localization signal motif that prevents PLSCR1's nuclear import. These data imply that the capacity of PLSCR1 to augment G-CSF-dependent granulopoiesis is unrelated to its reported activities at the endofacial surface of the plasma membrane, but does require entry of the protein into the nucleus. Consistent with this conclusion, nuclear-trafficking of PLSCR1 was observed in the granulocyte precursors in response to G-CSF stimulation. Whether this effect of nuclear PLSCR1 on increasing the emergency neutrophil production is directly mediated through its known capacity to activate transcription of IP3R1 (or potentially other genes) requires further investigation.
520 $a In summary, whereas facilitated differentiation of granulocytes is the best documented hematopoietic response initiated by G-CSF, this thesis elucidates a previously unidentified role of PLSCR1 in enhancing the "robustness" of the hematopoietic response to G-CSF, i.e. by increasing the amplification divisions of granulocyte precursors before their maturation into terminally differentiated neutrophils. This study for the first time also demonstrates a role for PLSCR1, a membrane-tethered protein, as a nuclear effector modulating G-CSF-induced emergency granulopoiesis. Results from this work extend our knowledge of the role of PLSCR1 in the complicated regulatory networks governing neutrophil development.
590 $a School code: 0188.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Pathology. $3 1017854
650 4 $a Health Sciences, Immunology. $3 1017716
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