Midkine: From Embryogenesis to Pathogenesis and Therapy by Takashi Muramatsu (auth.), Mine Ergüven, Takashi Muramatsu,

By Takashi Muramatsu (auth.), Mine Ergüven, Takashi Muramatsu, Ayhan Bilir (eds.)

Carl Edward Sagan’s (1934-1996) one of many recognized citation used to be “Who are we? we discover that we are living on a trifling planet of a run of the mill superstar misplaced in a galaxy tucked away in a few forgotten nook of a universe during which there are way more galaxies than people.“ From previous up to now, recognized molecules, enzymes, proteins, lipids and carbohydrates are studied within the pathogenesis of a number of illnesses either as a diagnostic/prognostic biomarker and healing agent. The underlying mechanism of unexplained illnesses and failure of remedies are usually studied with famous biomarkers, yet stay uncertain in lots of circumstances. As Dr. Sagan acknowledged different keys are nonetheless ready to be identified in a few forgotten nook of a physique universe, we discover power to suggest that one in every of them might be the expansion issue with cytokine task named “Midkine” This booklet summarizes the vast updated literature overeview with the lastest paintings of specialists approximately midkine in an in depth layout that conveys its function as either a pathologic issue and healing agent.

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The Smad complex may also induce expression of TWIST, SNAIL (SNAI1), and SLUG (SNAI2). The Smad complex 44 Y. A. Ratovitski can also induce Jagged1, which activates the Notch pathway, and CUTL1, which induces expression of the Wnt5 pathway leading to a b-catenin nuclear accumulation along with LEF1 [32]. The Smad complex also repressed the inhibitor of differentiation-2/3 expression leading to a subsequent E-cadherin down-regulation and EMT [32]. EGF-induced EMT was shown to be associated with both activation of SNAIL, thus causing the SNAI1-dependent repression of target genes and phosphorylation of STAT3, which can then transactivate the Twist promoter [32].

Both MDK and TP63 were shown to act as regulators of cell death and to be implicated in tumor cell response to chemotherapy [47, 48]. Thus, a potential link between MDK-induced and TP63-dependent pathways provides a new venue in developing of novel anticancer therapies. Tp63 is directly involved in the regulation of EMT in normal and pathological conditions, including tumor invasiveness [20, 35, 36, 38, 39, 49]. Knockdown of Tp63 expression (TAp63) caused down-regulation of cell adhesion-associated genes, cell detachment and anoikis (cell death associated with anchorage-dependent cells detaching from the surrounding extracellular matrix) in mammary epithelial cells and keratinocytes [36, 39].

Thus, the structure of MK resembles what could be regarded as a “tandem b-defensin”. Influence from Salt The antibacterial activity of many AMPs is drastically decreased when the ionic strength is increased, not least in cystic fibrosis as described by Goldman et al. [24]. Interestingly, we found that the antibacterial activity of MK was only slightly decreased in the presence of sodium chloride at physiologic concentrations, as described by Svensson et al. However, shorter linear fragments of the holoprotein lost most of their antibacterial activity in the presence of salt, suggesting that the rigid structure held together by disulphide bonds play a role for the salt-resistant activity of the holoprotein [19].

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