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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.
1

Rekombinante Analyse der N-terminalen Region von Laminin-[alpha]-Ketten [Laminin-alpha-Ketten]

Garbe, Jörg. January 2001 (has links) (PDF)
Hannover, Universiẗat, Diss., 2001.
2

Rekombinante Herstellung und Charakterisierung des E3-Fragments sowie seiner einzelnen Module LG4 und LG5 aus der Laminin-1-[alpha]1-Kette [Laminin-1-alpha1-Kette]

Andaç, Zeynep. January 2002 (has links)
Berlin, Freie Universiẗat, Diss., 2000. / Dateiformat: zip, Dateien im PDF-Format.
3

Rekombinante Mini-Laminin-5-Proteine zur Charakterisierung der 3 1-Integrin-Bindung [Alpha-3-Beta-1-Integrin-Bindung]

Künneken, Kerstin. January 2002 (has links)
Münster (Westfalen), Universiẗat, Diss., 2002. / Dateien im PDF-Format.
4

An investigation into the genes mediating myoblast migration in the nematode : Caenorhabditis elegans

Viveiros, Ryan 05 1900 (has links)
During C. elegans embryogenesis, myoblasts initially form two rows along the left and right lateral midlines and at ~290 min of development migrate dorsally and ventrally to form the four muscle quadrants present upon hatching (Sulston et al, 1983). As the myoblasts migrate they are still dividing, as are many other cells in their immediate environment. This means the cell-cell contact of cells during migration is dynamic and can vary from animal to animal (Schnabel et al, 1997). This situation creates an environment where the extracellular matrix (ECM) and cell surface contacts are in constant flux, which begs the questions as to how these cells navigate unerringly to their final destination. In an attempt to identify genes mediating these migrations, I performed an RNAi based screen targeting 776 genes predicted to be members of the extracellular matrix (ECM), or one of its receptors. Using both feeding and injection based RNAi, I was able to identify three genes of interest. Knockdowns of F56B3.2 resulted in paralyzed animals with detached muscle, making it a good candidate for a new component of the muscle attachment complex. F33G12.4 knockdowns resulted in an embryonic arrest phenotype with an abnormal muscle lineage, possibly stemming from polarity defects. The only knockdown that resulted in muscle migration defects was that for lam-2, which encodes for the laminin gamma subunit. Analysis of the lam-2 knockdown, as well as knockdowns for the other laminin subunits, revealed dorsal/ventral migration defects as well as a posterior displacement of the anterior-most ventral muscle cells. Investigation of this posterior displacement has led to the identification of a previously un-described anterior muscle migration event and its dependency upon the extension of muscle processes from the leading cells.
5

An investigation into the genes mediating myoblast migration in the nematode : Caenorhabditis elegans

Viveiros, Ryan 05 1900 (has links)
During C. elegans embryogenesis, myoblasts initially form two rows along the left and right lateral midlines and at ~290 min of development migrate dorsally and ventrally to form the four muscle quadrants present upon hatching (Sulston et al, 1983). As the myoblasts migrate they are still dividing, as are many other cells in their immediate environment. This means the cell-cell contact of cells during migration is dynamic and can vary from animal to animal (Schnabel et al, 1997). This situation creates an environment where the extracellular matrix (ECM) and cell surface contacts are in constant flux, which begs the questions as to how these cells navigate unerringly to their final destination. In an attempt to identify genes mediating these migrations, I performed an RNAi based screen targeting 776 genes predicted to be members of the extracellular matrix (ECM), or one of its receptors. Using both feeding and injection based RNAi, I was able to identify three genes of interest. Knockdowns of F56B3.2 resulted in paralyzed animals with detached muscle, making it a good candidate for a new component of the muscle attachment complex. F33G12.4 knockdowns resulted in an embryonic arrest phenotype with an abnormal muscle lineage, possibly stemming from polarity defects. The only knockdown that resulted in muscle migration defects was that for lam-2, which encodes for the laminin gamma subunit. Analysis of the lam-2 knockdown, as well as knockdowns for the other laminin subunits, revealed dorsal/ventral migration defects as well as a posterior displacement of the anterior-most ventral muscle cells. Investigation of this posterior displacement has led to the identification of a previously un-described anterior muscle migration event and its dependency upon the extension of muscle processes from the leading cells.
6

Biological roles of laminins 8, 9 and 10 /

Thyboll, Jill, January 2002 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 4 uppsatser.
7

On laminins and laminin receptors and their role in regeneration and myelination of the peripheral nerve /

Wallquist, Wilhelm, January 2004 (has links)
Diss. (sammanfattning) Stockholm : Karol inst., 2004. / Härtill 4 uppsatser.
8

Rekombinante Mini-Laminin-5-Proteine zur Charakterisierung der 3 1-Integrin-Bindung

Künneken, Kerstin. Unknown Date (has links)
Universiẗat, Diss., 2002--Münster (Westfalen). / Dateien im PDF-Format.
9

An investigation into the genes mediating myoblast migration in the nematode : Caenorhabditis elegans

Viveiros, Ryan 05 1900 (has links)
During C. elegans embryogenesis, myoblasts initially form two rows along the left and right lateral midlines and at ~290 min of development migrate dorsally and ventrally to form the four muscle quadrants present upon hatching (Sulston et al, 1983). As the myoblasts migrate they are still dividing, as are many other cells in their immediate environment. This means the cell-cell contact of cells during migration is dynamic and can vary from animal to animal (Schnabel et al, 1997). This situation creates an environment where the extracellular matrix (ECM) and cell surface contacts are in constant flux, which begs the questions as to how these cells navigate unerringly to their final destination. In an attempt to identify genes mediating these migrations, I performed an RNAi based screen targeting 776 genes predicted to be members of the extracellular matrix (ECM), or one of its receptors. Using both feeding and injection based RNAi, I was able to identify three genes of interest. Knockdowns of F56B3.2 resulted in paralyzed animals with detached muscle, making it a good candidate for a new component of the muscle attachment complex. F33G12.4 knockdowns resulted in an embryonic arrest phenotype with an abnormal muscle lineage, possibly stemming from polarity defects. The only knockdown that resulted in muscle migration defects was that for lam-2, which encodes for the laminin gamma subunit. Analysis of the lam-2 knockdown, as well as knockdowns for the other laminin subunits, revealed dorsal/ventral migration defects as well as a posterior displacement of the anterior-most ventral muscle cells. Investigation of this posterior displacement has led to the identification of a previously un-described anterior muscle migration event and its dependency upon the extension of muscle processes from the leading cells. / Medicine, Faculty of / Medical Genetics, Department of / Graduate
10

An investigation into the possible role of perlecan in pathogenesis of Alzeimer's disease

Liggins, Jason January 1999 (has links)
No description available.

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