Disease relevance of Mark1

• HIV and the cells it infects: sorting the latent from the labile. An interview with Mike McCune, MD, PhD. Interview by Mark Mascolini [1].

High impact information on Mark1

• As discussed by Mark Smyth and Joseph Trapani, the immediate molecular targets of perforin/granzyme-mediated apoptosis are still unclear, though candidate molecules with homology to cell death gene products from primitive organisms are currently under close scrutiny [2].
• During in vitro cultivation of the tissue, progenitor cells undergo osteogenic differentiation and form new bone (Silbermann, M., D. Lewinson, H. Gonen, M. A. Lizarbe, and K. von der Mark. 1983. Anat. Rec. 206:373-383) [3].
• In addition, mice completely deficient in annexin 2 display fibrin accumulation within blood vessels and impaired clearance of injury-induced thrombi (Ling Q., Jacovina, A.T., Deora, A.B., Febbraio, M., Simantov, R., Silverstein, R. L., Hempstead, B. L., Mark, W., and Hajjar, K. A. (2004) J. Clin. Investig. 113, 38-48) [4].
• Growing myotubes in myoblast cultures accumulate laminin and type IV collagen on their surface in patches and strands as the first step in assembling a continuous basal lamina on mature myofibers (U. Kühl, R. Timpl, and K. von der Mark (1982), Dev. Biol. 93, 344-359) [5].
• However, it has been noted that beta-amyloid accumulation is associated with markers of oxidative stress including protein oxidation (Smith et al., 1997), lipid peroxidation (Mark et al., 1997; Sayre et al., 1997), advanced glycation end products (Smith et al., 1994), and oxidation of nucleic acids (Nunomura et al., 1999) [6].

Biological context of Mark1

• In what follows I have begun to repay my indebtedness to my mentor Emil Witschi who introduced me to developmental biology, physiology, and genetics and its historical study on the basis of birds (and amphibians); and to Mark Leppert, Professor of Human Genetics at the University of Utah for collaborative support, and bird-watching fieldtrips [7].
• These results support the hypothesis that, in the tooth germ, chondroitin sulfate proteoglycans participate in the regulation of cell kinetic-dependent morphogenesis (Mark et al., 1990. Differentiation 43, 37-50) [8].

Associations of Mark1 with chemical compounds

• Dysprosium-166 (166Dy) was obtained by neutron irradiation of enriched 164Dy(2)O(3) in a Triga Mark III reactor [9].

References