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001 on1097606252;

003 OCoLC;

005 20190726095705.0;

006 m o d ;

007 cr unu||||||||;

008 190418s2018 ncua obm 000 0 eng d;

035 a| (Sirsi) o1097606252;

035 a| (OCoLC)1097606252;

049 a| EREE;

100 1 a| Velte, Ellen Kay,e| author.?| UNAUTHORIZED;

245 14 a| The role of differential sensitivity to retinoic acid (RA) in regulating spermatogonial fate /c| by Ellen Kay Velte.;

264 1 a| [Greenville, N.C.] :b| [East Carolina University],c| 2018.;

300 a| 131 pages :b| illustrations (chiefly color).;

336 a| textb| txt2| rdacontent;

337 a| computerb| c2| rdamedia;

338 a| online resourceb| cr2| rdacarrier;

347 a| text fileb| PDFc| 4.283 MB2| rda;

490 1 a| ECU Brody School of Medicine dissertation;

538 a| System requirements: Adobe Reader.;

538 a| Mode of access: World Wide Web.;

502 b| Ph.D.c| East Carolina Universityd| 2018.;

500 a| Presented to the Academic Faculty of the Department of Anatomy and Cell Biology;

500 a| Advisor: Christopher B. Geyer;

500 a| Title from PDF t.p. (viewed June 5, 2019).;

520 3 a| In the mammalian testis, the foundation of spermatogenesis is provided by spermatogonial stem cells (SSCs); their progeny either remain as stem cells (following a self-renewal division) or proliferate as undifferentiated progenitors prior to differentiating in response to retinoic acid (RA) and later entering meiosis. The mechanisms regulating spermatogonial response to RA are undefined, and their identification would represent a key advance in our understanding of how spermatogonial fate is determined both at the beginning of spermatogenesis and throughout the male reproductive lifespan. This dissertation summarizes the results of an investigation into elusive mechanisms regulating a key switch fundamental to spermatogonial fate, the capacity of spermatogonia to respond to RA. The results support a novel model by which mammalian prospermatogonial and spermatogonial fates are regulated by intrinsic capacity to respond (or not) to the differentiation signal provided by RA prior to and concurrent with the initiation of spermatogenesis.;

504 a| Includes bibliographical references.;

650 2 a| Spermatogonia.=| ^A1374356;

650 2 a| Tretinoin.=| ^A1289074;

650 2 a| Spermatogenesis.=| ^A919033;

653 a| retinoic acid;

653 a| testis;

653 a| CYP26;

653 a| talarozole;

700 1 a| Geyer, Christopher B.,e| degree supervisor.?| UNAUTHORIZED;

710 2 a| East Carolina University.b| Department of Anatomy and Cell Biology.?| UNAUTHORIZED;

830 0 a| ECU Brody School of Medicine dissertation.?| UNAUTHORIZED;

856 40 z| Access via ScholarShipu| http://hdl.handle.net/10342/7078;

949 o| wjh;

994 a| C0b| ERE;

096 a| WJ 834;

596 a| 1 4;

998 a| 5091134;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 5091134-1001l| JNETm| JOYNERr| Ys| Yt| JNE3ETDu| 4/18/2019x| ETDz| JERESOURCE;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 5091134-2001l| HSLELECm| HSLr| Ys| Yt| HEETDu| 4/18/2019x| ETDz| HERESOURCE;

The role of differential sensitivity to retinoic acid (RA) in regulating spermatogonial fate / by Ellen Kay Velte.

Author/creator	Velte, Ellen Kay author.
Other author	Geyer, Christopher B., degree supervisor.
Other author	East Carolina University. Department of Anatomy and Cell Biology.
Format	Theses and dissertations
Publication	[Greenville, N.C.] : [East Carolina University], 2018.
Description	131 pages : illustrations (chiefly color).
Supplemental Content	Access via ScholarShip
Subjects	Spermatogonia. Tretinoin. Spermatogenesis.

Series	ECU Brody School of Medicine dissertation ECU Brody School of Medicine dissertation. UNAUTHORIZED
Summary	In the mammalian testis, the foundation of spermatogenesis is provided by spermatogonial stem cells (SSCs); their progeny either remain as stem cells (following a self-renewal division) or proliferate as undifferentiated progenitors prior to differentiating in response to retinoic acid (RA) and later entering meiosis. The mechanisms regulating spermatogonial response to RA are undefined, and their identification would represent a key advance in our understanding of how spermatogonial fate is determined both at the beginning of spermatogenesis and throughout the male reproductive lifespan. This dissertation summarizes the results of an investigation into elusive mechanisms regulating a key switch fundamental to spermatogonial fate, the capacity of spermatogonia to respond to RA. The results support a novel model by which mammalian prospermatogonial and spermatogonial fates are regulated by intrinsic capacity to respond (or not) to the differentiation signal provided by RA prior to and concurrent with the initiation of spermatogenesis.
General note	Presented to the Academic Faculty of the Department of Anatomy and Cell Biology
General note	Advisor: Christopher B. Geyer
General note	Title from PDF t.p. (viewed June 5, 2019).
Dissertation note	Ph.D. East Carolina University 2018.
Bibliography note	Includes bibliographical references.
Technical details	System requirements: Adobe Reader.
Technical details	Mode of access: World Wide Web.

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The role of differential sensitivity to retinoic acid (RA) in regulating spermatogonial fate / by Ellen Kay Velte.

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