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You searched for subject:(Pi 3 k). Showing records 1 – 2 of 2 total matches.

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NSYSU

1. Huang, Kai-Lieh. Androgen Promotes Osteoblast Proliferation through Activation of Phosphatidylinositol-3-OH Kinase /Akt Signaling Pathway.

Degree: Master, Biological Sciences, 2003, NSYSU

Androgen has been shown to stimulate proliferation of osteoblast-like MC3T3-E1 cells. However, the molecular mechanism responsible for this effect remains to be elucidated. In the present study we demonstrate herein the non-genomic effect of androgen on osteoblast-like MC3T3-E1 cells involving activation of a PI(3)K/Akt signaling pathway and stimulating proliferation. In studies of steroids signaling, 5a-dihydrotestosterone (DHT), testosterone and 17b-estradiol but not dexamethasone or progesterone induced a rapid and transient phosphorylation of Akt in MC3T3-E1 cells. The androgen-induced Akt activation reached to the climax after 15 min and gradually diminished to baseline after 60 min. This induction of androgen was unaffected by actinomycin D and was specifically blocked by androgen receptor (AR) antagonist hydroxyflutamide (HF) or transfection of siRNA-AR. Treatment of MC3T3-E1 cells with PI(3)K inhibitor LY294002 or transfection with kinase-deficient Akt blocked androgen-induced cells proliferation. Moreover, androgen-induced activation of Akt was abolished by inhibitors of Src kinase, Gi-protein and phospholipase C showing the involvement of these effectors in androgen signaling pathway. Further, androgen-induced activation of Akt was dependent on intracellular calcium as shown by the effect of EGTA and intracellular calcium chelator BAPTA/AM. Fluorescence microscopy showed translocation of phospho-Akt from cytosol into nucleus after androgen treatment but no change in the subcellular distribution of phospho-Akt when HF or LY294002 pretreatment was administered to the cells. These results strongly suggest that phosphorylation of Akt in osteoblast cells is mediated by androgen receptor and the androgen-induced translocation of Akt is an important step in the androgen/AR signaling pathway that mediates osteoblast cells proliferation. Advisors/Committee Members: Chung-Lung Cho (committee member), Jiin-Tsuey Cheng (chair), Hong-Yo Kang (committee member), Michael Hsiao (chair).

Subjects/Keywords: Akt; PI(3)K; proliferation; androgen; osteoblast

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Huang, K. (2003). Androgen Promotes Osteoblast Proliferation through Activation of Phosphatidylinositol-3-OH Kinase /Akt Signaling Pathway. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0708103-151701

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Huang, Kai-Lieh. “Androgen Promotes Osteoblast Proliferation through Activation of Phosphatidylinositol-3-OH Kinase /Akt Signaling Pathway.” 2003. Thesis, NSYSU. Accessed April 10, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0708103-151701.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Huang, Kai-Lieh. “Androgen Promotes Osteoblast Proliferation through Activation of Phosphatidylinositol-3-OH Kinase /Akt Signaling Pathway.” 2003. Web. 10 Apr 2021.

Vancouver:

Huang K. Androgen Promotes Osteoblast Proliferation through Activation of Phosphatidylinositol-3-OH Kinase /Akt Signaling Pathway. [Internet] [Thesis]. NSYSU; 2003. [cited 2021 Apr 10]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0708103-151701.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Huang K. Androgen Promotes Osteoblast Proliferation through Activation of Phosphatidylinositol-3-OH Kinase /Akt Signaling Pathway. [Thesis]. NSYSU; 2003. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0708103-151701

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Michigan

2. Zell, Traci. Two mechanisms of beta1 integrin regulation in human leukocytes.

Degree: PhD, Molecular biology, 1997, University of Michigan

Cell adhesion plays a fundamental role in controlling normal cellular behavior. Integrins are a large family of adhesion molecules that play an important role in mediating lymphocyte interactions with other cells and with components of the extracellular matrix. The distinct array of integrins expressed on the surface of a cell at any given time dictate the spectrum of ECM and cell surface ligands with which the cell can interact. Changes in integrin expression can dramatically affect lymphocyte recirculation and activation. Unlike most cell types in the body that continuously stay in a distinct anatomical location, cells of the immune system require the ability to alternate between adhesive and nonadhesive states in order to function properly. Normal lymphocyte recirculation requires that cells be in a relatively nonadherent state so that rapid movement throughout the vascular and lymphatic systems is not impeded. Movement of cells into peripheral lymphoid organs and other tissues, where antigen recognition occurs, involves a multi-step adhesion process that allows circulating cells to slow down and extravasate through the vascular endothelium. This thesis addresses two important mechanisms that influence lymphocyte adhesion: (1) regulation of cell surface β1 integrin expression and (2) activation-dependent regulation of β1 integrin function. Results using normal Jurkat T cells and α4-deficient Jurkat cells have suggested potential mechanisms that might be used by lymphocytes to regulate cell surface expression of β1 integrins. These studies indicate that expression of individual α subunits may be regulated differently in lymphocytes. Our results suggest a role for both post-transcriptional and post-translation control of α2 subunit protein expression and a role for post-transcriptional regulation of the α5 subunit. In addition, re-expression experiments suggest that the presence of α4 protein may influence cell surface expression of other a subunits. Studies with HL60 transfectants expressing CD2/28 chimeric receptors have implicated phosphatidylinositol 3-kinase (PI 3-K) as playing an important role in the ability of CD28 to regulate integrin-mediated adhesion. However, substitution of the CD28 SH2-binding motif YMNM with the YVKM motif from CTLA-4 indicated that recruitment and activation of PI 3-K is not a sufficient signal to upregulate β1 integrin-mediated adhesion since this receptor could still mediate PI 3-K activation but not integrin upregulation. Advisors/Committee Members: Shimizu, Yoji (advisor), Koomey, J. Michael (advisor).

Subjects/Keywords: Adhesion; Beta1; Human; Integrin; Leukocytes; Mechanisms; Pi 3-k; Regulation; Two

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Zell, T. (1997). Two mechanisms of beta1 integrin regulation in human leukocytes. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/130404

Chicago Manual of Style (16th Edition):

Zell, Traci. “Two mechanisms of beta1 integrin regulation in human leukocytes.” 1997. Doctoral Dissertation, University of Michigan. Accessed April 10, 2021. http://hdl.handle.net/2027.42/130404.

MLA Handbook (7th Edition):

Zell, Traci. “Two mechanisms of beta1 integrin regulation in human leukocytes.” 1997. Web. 10 Apr 2021.

Vancouver:

Zell T. Two mechanisms of beta1 integrin regulation in human leukocytes. [Internet] [Doctoral dissertation]. University of Michigan; 1997. [cited 2021 Apr 10]. Available from: http://hdl.handle.net/2027.42/130404.

Council of Science Editors:

Zell T. Two mechanisms of beta1 integrin regulation in human leukocytes. [Doctoral Dissertation]. University of Michigan; 1997. Available from: http://hdl.handle.net/2027.42/130404

.