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Muscle transcription factors

Fig. 2 Mesenchymal stem cell differentiation on substrates with different elasticity (a-c) neurogenic differentiation on soft matrices (d-f) myogenic matrices showing upregulated muscle transcription factor (g—i) osteogenic differentiation on stiffer matrices. Reproduced with permission from Engler et al. [35]... Fig. 2 Mesenchymal stem cell differentiation on substrates with different elasticity (a-c) neurogenic differentiation on soft matrices (d-f) myogenic matrices showing upregulated muscle transcription factor (g—i) osteogenic differentiation on stiffer matrices. Reproduced with permission from Engler et al. [35]...
Ca2+-binding Proteins Smooth Muscle Tone Regulation NPAT Family of Transcription Factors... [Pg.311]

NFAT2 plays a key role in the development of the embryo s heart. In the precursor cells, there is a temporal and spatial specific expression of NFAT2, which directs the formation of the valves and the septum in the heart. In the adult heart, NFAT proteins also cooperate with transcription factors of the GATA and MEF2 families to regulate cardiac muscle hypertrophic responses. [Pg.849]

Two additional parasite proteins with apparent HLH binding properties were identified, based on the idea that direct antagonism of host HLH transcription factors might be responsible for muscle cell subversion. One is a MyoDdike protein (Connolly el al., 1996) and another (110 kDa) is located in the vicinity of the hypodermis or somatic musculature of muscle larvae (Lindh el al., 1998). Secretion of these proteins into the infected cell has not been reported. [Pg.140]

These agents activate PPAR-y a nuclear transcription factor important in fat cell differentiation and fatty acid metabolism. PPAR-yagonists enhance insulin sensitivity in muscle, liver, and fat tissues indirectly. Insulin must be present in significant quantities for these actions to occur. [Pg.231]

Nelson There are three separate roles for Ca2+ waves. First, delivering Ca2+ for contraction. Second, modulating Ca2+ dependent ion channels that control the membrane potentials. Depending on the tissue this can involve BK channels, SK channels or Ca2+-activated Cl- channels. Third, controlling Ca2+-dependent transcription factors. There is quite clear evidence that the frequency and the amplitude components of the Ca2+ signals can determine which Ca2+-dependent transcription factors are activated. This can encode both short and long-term information to control smooth muscle function. [Pg.272]

Puri, P.L. and Sartorelli, V. (2000) Regulation of muscle regulatory factors by DNA-binding, interacting proteins, and post-transcriptional modifications, /ourmil of Cellular Physiology, 185, 155-173. [Pg.95]

TNF-a is identical to cachetin, a protein that suppresses completely the lipoprotein lipase of adipose tissue and is believed to be responsible for cachexia, a condition of general ill health, malnutrition, weight loss, and wasting of muscle that accompanies cancer and other chronic diseases. Nevertheless, TNF-a may be overproduced in obesity as well. It has been suggested that abnormal production of TNF-a may induce cachexia while abnormal action of the cytokine may cause obesity.233 Some TNF receptors have "death domains" and trigger apoptosis, while other receptors promote proliferation and differentiation via transcription factor NF-kB.242... [Pg.1849]

Muscle, whose structure and function are discussed in Chapter 19, develops in response to four members of the myoD family. These include myoD, myogenin, myf5, and MRF4.417-419 All are muscle-specific transcription factors of the basic helix -loop -helix class. An unusual aspect of muscle development is formation of multinucleate myotubes (muscle fibers p. 1096)420 Apoptosis plays an important role in muscle development and can present significant complications in damaged cardiac muscle.421 Defects in several developmental control genes are responsible for congenital heart diseases.422... [Pg.1902]


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