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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
41

The role of PTF1A in spinal cord development

Glasgow, Stacey Marie. January 2006 (has links)
Thesis (Ph.D.) -- University of Texas Southwestern Medical Center at Dallas, 2006. / Embargoed. Vita. Bibliography: 121-142.
42

A Multiparameter Network Reveals Extensive Divergence Between <em>C. elegans</em> bHLH Transcription Factors: A Dissertation

Grove, Christian A. 11 September 2009 (has links)
It has become increasingly clear that transcription factors (TFs) play crucial roles in the development and day-to-day homeostasis that all biological systems experience. TFs target particular genes in a genome, at the appropriate place and time, to regulate their expression so as to elicit the most appropriate biological response from a cell or multicellular organism. TFs can often be grouped into families based on the presence of similar DNA binding domains, and these families are believed to have expanded and diverged throughout evolution by several rounds of gene duplication and mutation. The extent to which TFs within a family have functionally diverged, however, has remained unclear. We propose that systematic analysis of multiple aspects, or parameters, of TF functionality for entire families of TFs could provide clues as to how divergent paralogous TFs really are. We present here a multiparameter integrated network of the activity of the basic helix-loop-helix (bHLH) TFs from the nematode Caenorhabditis elegans. Our data, and the resulting network, indicate that several parameters of bHLH function contribute to their divergence and that many bHLH TFs and their associated parameters exhibit a wide range of connectivity in the network, some being uniquely associated to one another, whereas others are highly connected to multiple parameter associations. We find that 34 bHLH proteins dimerize to form 30 bHLH dimers, which are expressed in a wide range of tissues and cell types, particularly during the development of the nematode. These dimers bind to E-Box DNA sequences and E-Box-like sequences with specificity for nucleotides central to and flanking those E-Boxes and related sequences. Our integrated network is the first such network for a multicellular organism, describing the dimerization specificity, spatiotemporal expression patterns, and DNA binding specificities of an entire family of TFs. The network elucidates the state of bHLH TF divergence in C. elegans with respect to multiple functional parameters and suggests that each bHLH TF, despite many molecular similarities, is distinct from its family members. This functional distinction may indeed explain how TFs from a single family can acquire different biological functions despite descending from common genetic ancestry.
43

Differential circadian regulation of Bmal1 transcription by orphan nuclear receptors

Ruan, Xuan, 1974- January 2008 (has links)
No description available.
44

The Identification of Cooperating Mutations in TAL1-Mediated Leukemia in the Mouse: A Dissertation

Calvo, Jennifer Ann 01 September 2005 (has links)
A sequential series of mutational events is necessary for the development of leukemia. The misexpression of TAL1, a basic helix-loop-helix (bHLH) transcription factor, is the most common mutation in T cell acute lymphoblastic leukemia (T-ALL). Tal1 transgenic mice develop leukemia with a long latency and incomplete penetrance indicating additional mutations are necessary to develop disease. To investigate additional mutational events that potentially contribute to TAL1-expressing T-ALL patients, we sought to identify cooperating mutations in Tal1 transgenic mice. Clinical studies implicated the loss of the INK4a/ARF locus, which encodes two tumor suppressors, p16INK4a and p14ARF, in the majority of T-ALL patients. We demonstrated disease acceleration in tal1/ink4a/arf+/-, tal1/pl6ink4a+/- and tal1/p19arf+/- mice, thereby providing genetic evidence that Tal1 cooperates with loss of either p16Ink4a or p19Arf in leukemogenesis. The cooperation of Tal1 with the loss of or p16Ink4a or p19Arf, is consistent with our observation that Tal1 alters cell cycle regulation in leukemia by promoting S phase induction and apoptosis in vivo. An additional mutational event common in tal1 tumors is activation of the Notch1 signaling pathway. We provide evidence that the majority of tal1 tumors express increased levels of Notch1, and exhibit activating notch1 mutations. Additionally, tal1 tumors display sensitivity to the pharmacologic inhibition of γ-secretase activity in vitro, indicating that γ-secretase inhibitors may prove an efficacious treatment for TAL1-expressing T-ALL patients. Furthermore, we developed a doxycycline-regulated NotchIC T-ALL cell line, which will allow the identification of important Notch1IC target genes in leukemogenesis.
45

The effect of scleraxis-transduced tendon-derived stem cells (TDSCs) on tendon repair in a rat model.

January 2013 (has links)
我們假設,將scleraxis (Scx)基因轉導入肌腱來源的幹細胞(TDSC),製成TDSC-Scx細胞系。TDSC-Scx會促進肌腱修復。本研究的目的在於探索Scx促進TDSC成肌腱分化的作用,以及TDSC-Scx對肌腱修復的促進作用。 / 使用慢病毒載體將Scx轉導入TDSCs,不含Scx的空載作為對照也轉導入TDSCs,用載體上帶有的抗性基因,殺稻瘟菌素對細胞進行篩選。分別建成TDSC-Scx和TDSC-Mock細胞系。Scx 的表達分別用定量PCR以及免疫螢光在mRNA和蛋白水準進行鑒定。TDSC-Scx成肌腱,成軟骨和成骨方向的分化能力用定量PCR檢驗。用大鼠臏腱視窗損傷模型進行了細胞移植試驗,測試TDSC-Scx對肌腱損傷的修復作用。實驗分為三組:(1)支架組,(2)空載體組,(3)Scx組。在細胞移植後的第二,四,八周,收集正在修復中的肌腱樣品,進行植入細胞的存留狀態,鈣化,組織學和生物力學測驗。 / TDSC-Scx比TDSC-Mock有更強的成肌腱分化能力。但是,在成軟骨-成骨分化方面,沒有結論。在動物試驗,植入的細胞在第二周仍然可見,但自第四周起,就不見了。在第八周,各組均有個別樣品輕微異位鈣化,但各組別間並無顯著差異。在早期,TDSC-Scx組比空載體組和支架組合得來更好的修復肌腱的能力。 / TDSC-Scx可能促進肌腱損傷的早期修復。 / We hypothesized that transduction of tendon-derived stem cell (TDSC) with scleraxis (Scx) might promote its tenogenic differentiation and promote better tendon repair compared to TDSC without Scx transduction. This study thus aimed to investigate the effect of Scx transduction on the tenogenic differentiation of TDSC and the effect of the resulting cell line in the promotion of tendon repair. / TDSCs were transduced with lentivirus-mediated Scx or empty vector and selected by blasticidin. The mRNA and protein expression of Scx were checked by qRT-PCR and Immuno fluorescence, respectively. The expression of different lineage markers were examined by qRT-PCR. A rat patellar tendon window injury model was used. The operated rats were divided into 3 groups: (1) scaffold-only group, (2) TDSC-Mock group and (3) TDSC-Scx group. At week 2, 4 and 8 post-transplantation, the repaired patellar tendon was harvested for ex vivo fluorescent imaging, vivaCT imaging, histology, or biomechanical test. / TDSC-Scx consistently showed higher expression of tendon-related markers compared to TDSC-Mock. However, the effect of Scx transduction on the expression of chondro-osteogenic markers was less conclusive. The transplanted TDSCs could be detected in the window wound at week 2 but not at week 4. Ectopic ossification was detected in some samples at week 8 but there was no difference among different groups. The TDSC-Scx group promoted early tendon repair histologically and biomechanically compared to the scaffold-only group and the TDSC-Mock group. / TDSC-Scx might be used for the promotion of early tendon repair. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Tan, Chunlai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2013. / Includes bibliographical references (leaves 66-70). / Abstracts also in Chinese. / Chapter Thesis/Assessment Committee --- p.i / Acknowledgment --- p.ii / Publication --- p.vi / Abstract --- p.vii / 摘要 --- p.viii / Chapter Chapter 1 --- Tendon injury and tendon tissue engineering --- p.1 / Chapter 1.1 --- Anatomy of tendon --- p.1 / Chapter 1.2 --- Epidemiology of tendon injury --- p.3 / Chapter 1.3 --- Process and problems of tendon healing --- p.4 / Chapter 1.4 --- Current treatment and cell-based therapy for tendon repair --- p.5 / Chapter 1.5 --- Transcriptional factor Scleraxis and tendon --- p.8 / Chapter 1.5.1 --- Helix-loop-helix (HLH) and bHLH proteins --- p.8 / Chapter 1.5.2 --- Scleraxis --- p.9 / Chapter 1.6 --- Research focus and implications --- p.11 / Chapter 1.7 --- Hypotheses and objectives of this study --- p.12 / Chapter 1.8 --- Clinical significance --- p.13 / Chapter Chapter 2 --- Materials and Methods --- p.14 / Chapter 2.1 --- Study Design --- p.14 / Chapter 2.2 --- Establishment of TDSC-Scx cell line --- p.15 / Chapter 2.2.1 --- Isolation of TDSC and cell culture --- p.15 / Chapter 2.2.2 --- Establishment of TDSC-Scx cell line --- p.17 / Chapter 2.2.2.1 --- Construction of plasmid --- p.17 / Chapter 2.2.2.2 --- Transfection --- p.23 / Chapter 2.2.2.3 --- Infection --- p.24 / Chapter 2.2.2.4 --- Selection --- p.24 / Chapter 2.2.2.5 --- Characterization of TDSC-Scx and TDSC-Mock --- p.25 / Chapter 2.2.2.5.1 --- qRT-PCR --- p.25 / Chapter 2.2.2.5.2 --- Immune-fluorescent (IF) --- p.26 / Chapter 2.2.2.6 --- Lineage marker expression --- p.26 / Chapter 2.2.3 --- Data analysis --- p.29 / Chapter 2.3 --- The effect of TDSC-Scx on healing in a patellar tendon window injury model --- p.30 / Chapter 2.3.1 --- Animal surgery --- p.30 / Chapter 2.3.2 --- Ex Vivo Fluorescence Imaging --- p.32 / Chapter 2.3.3 --- vivaCT --- p.33 / Chapter 2.3.4 --- Histology --- p.33 / Chapter 2.3.5 --- Biomechanical test --- p.35 / Chapter 2.3.6 --- Data analysis --- p.37 / Chapter Chapter 3 --- Results --- p.38 / Chapter 3.1 --- Generation of TDSC-Scx and TDSC-Mock cell lines --- p.38 / Chapter 3.1.1 --- Plasmid --- p.38 / Chapter 3.1.2 --- Cell morphology --- p.38 / Chapter 3.1.3 --- Expression of Scx --- p.38 / Chapter 3.1.4 --- Expression of chondro-/osteo-/tenogenic markers --- p.39 / Chapter 3.2 --- The healing effect of TDSC-Scx on a patella tendon window injury model --- p.40 / Chapter 3.2.1 --- The fate of transplanted cells --- p.40 / Chapter 3.2.2 --- Ossification --- p.40 / Chapter 3.2.3 --- Histology --- p.40 / Chapter 3.2.3.1 --- Fiber arrangement --- p.41 / Chapter 3.2.3.2 --- Cellularity --- p.41 / Chapter 3.2.3.3 --- Cell alignment --- p.42 / Chapter 3.2.3.4 --- Cell rounding --- p.42 / Chapter 3.2.3.5 --- Vascularity --- p.43 / Chapter 3.2.3.6 --- Fiber structure --- p.43 / Chapter 3.2.3.7 --- Hyaline degeneration --- p.43 / Chapter 3.2.3.8 --- Inflammation --- p.44 / Chapter 3.2.3.9 --- Ossification --- p.44 / Chapter 3.2.4 --- Biomechanical properties --- p.44 / Chapter Chapter 4 --- Discussion --- p.55 / Chapter 4.1 --- In vitro --- p.55 / Chapter 4.1.1 --- Scx transduction did not lead to morphological change in TDSCs --- p.55 / Chapter 4.1.2 --- Scx transduction led to higher expression of Scx mRNA --- p.55 / Chapter 4.1.3 --- TDSC-Scx expressed higher levels of tenogenic markers --- p.56 / Chapter 4.2 --- In vivo --- p.58 / Chapter 4.2.1 --- The fate of transplanted cells --- p.58 / Chapter 4.2.2 --- Ossification was vague --- p.58 / Chapter 4.2.3 --- TDSC-Scx promoted tendon healing --- p.58 / Chapter 4.2.4 --- Biomechanical properties --- p.59 / Chapter 4.2.5 --- Clinical consideration --- p.60 / Chapter 4.3 --- Similar studies --- p.61 / Chapter Chapter 5 --- Limitations --- p.63 / Chapter 5.1 --- Direct Scx protein expression and function information unavailable --- p.63 / Chapter 5.2 --- Differentiation assay --- p.64 / Chapter Chapter 6 --- Conclusion --- p.65 / Reference --- p.66 / Appendix --- p.71
46

Pancreatic Endocrine Tumourigenesis : Genes of potential importance /

Johansson, Térèse A., January 2008 (has links)
Diss. (sammanfattning) Uppsala : Uppsala universitet, 2008.
47

Studies on the regulation of the Napin napA promoter by ABI3, bZIP and bHLH transcription factors /

Martin, Nathalie, January 2008 (has links)
Diss. (sammanfattning) Uppsala : Uppsala universitet, 2008. / Härtill 3 uppsatser.
48

GATA co-factors : collaborators in cardiac development, conspirators in cardiac disease

Kathiriya, Irfan S. January 2005 (has links) (PDF)
Thesis (Ph. D.) -- University of Texas Southwestern Medical Center at Dallas, 2005. / Vita. Bibliography: 70-86.
49

The role of bHLH gene ash1 in the developing chick eye

Mao, Weiming. January 2008 (has links) (PDF)
Thesis (Ph.D.)--University of Alabama at Birmingham, 2008. / Title from PDF title page (viewed on Sept. 17, 2009). Includes bibliographical references.
50

Diverse mechanisms employed by bHLH transcription factors to downregulate gene expression /

Rosenberg, Miriam Isaaca. January 2005 (has links)
Thesis (Ph. D.)--University of Washington, 2005. / Vita. Includes bibliographical references (leaves 91-100).

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