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You searched for subject:(Dlk protein). Showing records 1 – 2 of 2 total matches.

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NSYSU

1. Wu, Chia-Ling. The effect of Dlk overexpression on the tumorigenicity of hepatoma cells.

Degree: Master, Biological Sciences, 2004, NSYSU

Dlk is a transmembrane protein that possesses six epidermal growth factor-like sequences at the extracellular domain, a single transmembrane domain and an intracellular tail. The extracellular EFG-like region of Dlk can be released by action of an unknown protease that cuts the extracellular region near the cell membrane. Dlk belongs to the EGF-like homeotic protein family and has received many names: pG2, FA-1, Pref-1, SCP-1, ZOG and Dlk. All the proteins are identical or polymorphic products of a single gene. Dlk has been involved in several differentiation processes, such as adipogenesis, hematopoiesis and neuroendocrine differentiation. Dlk is also known as the preadipocyte factor-1 (Pref-1), is highly expressed in preadipocytes but is completely abolished in adipocytes. Pref-1 may function in the maintenance of the preadipocyte state and is a negative regulator of adipocyte differentiation. Dlk is expressed in tumors with neuroendocrine features, such as human neuroblastoma, rat pheochromocytoma, and a subset of Small Cell Lung Cancer (SCLC) cell lines. The Dlk expression is probably associated with some differentiation stages because the most undifferentiated cells were lacking expression of Dlk. The finding suggests that Dlk plays an important role in differentiation and tumorigenesis of several cell types. The study was designed to examine the influence of dlk overexpression on tumorigenicity of hepatoma cells. We constructed the mammalian expression vectors for full-length dlk, dlk extracellular domain, which were transfected into SK-Hep-1 cells for generation of stable clones. The transgene expressions in selected stable clones were verified by QRT-PCR and western blot analysis. Our results indicated that overexpression of extracellular domain significantly promoted the viability of SK-Hep1 cells during serum deprivation. In SCID mice, injection of full-length dlk clones led to increased tumor growth compared with the control groups. However, the migration ability was reduced in Dlk stable clones. In summary, these results suggested full-length Dlk promoted the tumor growth but reduced the migration ability of SK-Hep1 cells. Advisors/Committee Members: Cho Chung-Lung (chair), Tai Ming-Hong (committee member), Cheng Jiin-Tsuey (chair), Chuang Jiin-Haur (committee member).

Subjects/Keywords: overexpression; tumorigenicity; hepatoma cells; Dlk protein

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

APA (6th Edition):

Wu, C. (2004). The effect of Dlk overexpression on the tumorigenicity of hepatoma cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904104-203607

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):

Wu, Chia-Ling. “The effect of Dlk overexpression on the tumorigenicity of hepatoma cells.” 2004. Thesis, NSYSU. Accessed March 05, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904104-203607.

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

MLA Handbook (7th Edition):

Wu, Chia-Ling. “The effect of Dlk overexpression on the tumorigenicity of hepatoma cells.” 2004. Web. 05 Mar 2021.

Vancouver:

Wu C. The effect of Dlk overexpression on the tumorigenicity of hepatoma cells. [Internet] [Thesis]. NSYSU; 2004. [cited 2021 Mar 05]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904104-203607.

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

Council of Science Editors:

Wu C. The effect of Dlk overexpression on the tumorigenicity of hepatoma cells. [Thesis]. NSYSU; 2004. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904104-203607

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


University of Michigan

2. Li, Jiaxing. Restraint of the Wallenda/DLK MAP Kinase cascade by the Kinesin-3 motor regulates the assembly of synapses.

Degree: PhD, Molecular, Cellular, and Developmental Biology, 2017, University of Michigan

Synaptic connections are fundamental units of neuronal communication in the brain. They are composed of precisely opposed pre- and postsynaptic specializations, and these structures are dynamically regulated to adapt to changing needs of neuronal circuits. While mechanisms that regulate the postsynaptic composition of synapses are highly studied, less is known about presynaptic regulation. Within presynaptic terminals, synapse assembly requires the formation of active zones (AZs) and synaptic vesicle (SV) release machinery at synapses. An important role in presynaptic assembly has been assigned to a kinesin-3 family member, Unc-104/Imac/KIF1A. Unc-104/Imac/KIF1A is required for the delivery of synaptic components and SVs to nascent synapses. However, its distinct synaptic phenotype from other kinesins and the complexity of the phenotype is not well understood. This thesis work describes how the synaptic defects of Drosophila unc-104 mutants can be rescued by inhibiting the Wallenda (Wnd)/DLK MAP kinase signaling pathway. This pathway has been previously identified as a regulator of axonal damage signaling and presynaptic terminal morphology. The accessible genetic tools in Drosophila (reviewed in Chapter II) allow for characterization of the mechanistic relationship between Wnd/DLK and Unc-104. Wnd/DLK signaling becomes activated in unc-104 mutants, and inhibits synapse formation independently of Unc-104’s transport functions by controlling the levels and timing of the expression of AZ and SV components (Chapter III). In order to understand the activation mechanism of Wnd signaling, multiple possibilities have been examined (Chapter IV). Cumulative findings lead to a model that accumulated presynaptic proteins in the cell body of unc-104 mutants triggers the Wnd signaling pathway, which then down-regulates presynaptic protein levels. In this fashion Wnd signaling may function as a stress response pathway that regulates the expression level of synaptic proteins according to their ability to be transported in axons. This model also raises an interesting possibility that DLK activation may contribute to synapse malfunction and loss in the aged or diseased nervous system. Advisors/Committee Members: Collins, Catherine A (committee member), Pierchala, Brian Anthony (committee member), Hume, Richard I (committee member), Shafer, Orie (committee member), Xu, Haoxing (committee member).

Subjects/Keywords: kinesin-3; synapse; Wnd/DLK; presynaptic protein; axonal transport; development and maintenance; Molecular, Cellular and Developmental Biology; Science

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

APA (6th Edition):

Li, J. (2017). Restraint of the Wallenda/DLK MAP Kinase cascade by the Kinesin-3 motor regulates the assembly of synapses. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/137169

Chicago Manual of Style (16th Edition):

Li, Jiaxing. “Restraint of the Wallenda/DLK MAP Kinase cascade by the Kinesin-3 motor regulates the assembly of synapses.” 2017. Doctoral Dissertation, University of Michigan. Accessed March 05, 2021. http://hdl.handle.net/2027.42/137169.

MLA Handbook (7th Edition):

Li, Jiaxing. “Restraint of the Wallenda/DLK MAP Kinase cascade by the Kinesin-3 motor regulates the assembly of synapses.” 2017. Web. 05 Mar 2021.

Vancouver:

Li J. Restraint of the Wallenda/DLK MAP Kinase cascade by the Kinesin-3 motor regulates the assembly of synapses. [Internet] [Doctoral dissertation]. University of Michigan; 2017. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2027.42/137169.

Council of Science Editors:

Li J. Restraint of the Wallenda/DLK MAP Kinase cascade by the Kinesin-3 motor regulates the assembly of synapses. [Doctoral Dissertation]. University of Michigan; 2017. Available from: http://hdl.handle.net/2027.42/137169

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