Differentiation-inhibiting factor

Differentiation inhibiting factor and cartilage-inducing factor... 

In the EST, two murine cell lines are used to assess teratogenic potential the embryonic D3 stem cell (ES) which represents the embryonic tissue and the 3T3 fibroblast cell which represents the adult tissue. The D3 cells are maintained in an undifferentiated stage in the presence of leukemia inhibiting factor (LIE), then released from LIE and allowed to form embryo bodies that differentiate into cardiomyocytes. The D3 and 3T3 cells are exposed to a range of concentrations of the test ingredient. After a 10-day... 

Although the mechanism of action of IFN-a against HCL is incompletely understood, it most likely relates to IFN-a-induced B-cell differentiation, inhibition of hairy-cell responsiveness to B-cell growth factors, or activation of antineoplastic immune cell function [83]. 

A large number of 13C NMR studies on proline derivatives and proline peptides have appeared in the literature [815-830]. As the electron charge density of cis-proline carbons is different from that of franx-prolinc carbons, these isomers can be differentiated by nCNMR spectroscopy [826, 830]. On the basis of calculations Tonelli [831] predicted four conformations for the dipeptide Boc-Pro-Pro-OBzl, three of which could be detected by 13C NMR spectroscopy [826, 830], In proline-containing peptides the stereochemistry of the proline residue plays an important role for the conformation of these oligomers. The 13C chemical shift data of cis and trans proline derivatives, collected in Table 5.29, are useful to determine the stereochemistry of the amino acid-proline bond, e.g. in cyclo-(Pro-Gly)3, melanocyte-stimulating hormone release-inhibiting factor or thyrotropin-releasing hormone. 

Fig. 10.5 Osteoclast differentiation factors. Osteoblasts make monocyte colony stimulating factor (mCSF) that induces bone adherent monocytes carrying the corresponding receptor (mCSF Receptor) to fuse into osteoclast precursors (preosteoclasts). Preosteoclasts develop within the periosteum and are detectable by their expression of the osteoclast differentiation and activation receptor (ODAR). Osteoblasts also make cell-membrane bound and soluble osteoclast differentiation factors (ODF and sODF) that react with ODAR to cause preosteoclast differentiation. Finally, osteoblasts make osteoclast inhibition factor (OCIF), also called osteoprotegerin, which acts as an ODF decoy receptor and prevents ODF or sODF reacting with ODAR. ODAR is commonly referred to as RANK and ODF as the RANK ligand (RANKL) in the literature (see text)...

Leary, A.G., Wong, G.G., Clark, S.C., Smith, A.G. and Ogawa, M. (1990) Leukemia inhibitory factor differentiation-inhibiting activity/human interleukin for DA cells augments proliferation of human hematopoietic stem cells. BloodlS 1960-1964. 

Fig. 1. Oxidation hypothesis. Proposes minimally modified LDL is formed due to oxidation in the arterial intimal space. This LDL can still be taken up by the LDL receptor, but minimally modified LDL promotes release of proinflammatory mediators from monocytes and acts as a monocyte inhibition factor (MIF), reducing the motility of monocytes and thus leading to recruitment of macrophages (J4, W9). Macrophages further oxidize LDL (OxLDL), release inflammatory mediators, and rapidly take up OxLDL and other lipoproteins via the unregulated scavenger receptor that binds modified apo B to form lipid-laden foam cells. OxLDL is cytotoxic to a variety of cells in culture and may disrupt endothelial tissue, causing the release of inflammatory mediators and the entry of more LDL into the intimal space. Continued accumulation of monocytes and their differentiation into macrophages leads to a vicious cycle (J4, W9). Adapted from reference J4.

Fukuzawa T, Bagnara JT (1989) Control of Melanoblast Differentiation in Amphiba by Q-Melanocyte Stimulating Hormone, a Serum Melanization Factor, and a Melanization Inhibiting Factor. Pigment Cell Res 2 171... 

Fig. 3 shows that T cell receptor expression was partially inhibited at aU concentrations tested. Interestingly, thymocyte proliferation was also reduced with the inhibitor at concentrations of 0.5 mM and above. It is possible that this inhibition of proliferation was itself the result of inhibition of differentiation, as thymocyte growth appears to be stimulated by interleukin-2 and the most likely sources of this growth factor within the thymus are the thymocytes at a more advanced stage at differentiation. Inhibition of thymocyte maturation is therefore likely to reduce proliferation through die reduction in interleukin-2 production. 

Shoshan V and Shavit N (1979) ATP synthesis and hydrolysis in chloroplast membranes. Differential inhibition by antibodies to chloroplast coupling factor 1. Eur. J. Biochem. 94, 87-92. 

The anthrax toxin is a tripartite toxin and consists ofthe binding component protective antigen (PA), the lethal factor (LF), which is a metalloprotease, and the edema factor (EF), which is a calmodulin-dependent adenylyl-cyclase. Both enzyme components are translocated via PA into target cells. PA is activated by furin-induced cleavage and forms heptamers, which are similar to the binding components of C2 toxin and iota toxin. In the low pH compartment of endosomes, the heptamers form pores to allow translocation of LF and EF. LF cleaves six of the seven MEKs (MAPK-kinases) thereby inhibiting these enzymes. The functional consequence is the blockade of the MAPK pathways that control cell proliferation, differentiation, inflammation, stress response, and survival. Whether this is the reason for the LT-induced cell death of macrophages is not clear [1]. 

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