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发布于:2020-7-8 20:36:34  访问:69 次 回复:0 篇
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Ndothelial Cell Sources Has Different Binding Affinities For FGF2 [46]. These Data
Ndothelial cell sources has different binding affinities for FGF2 [46]. These data initially suggested that the protein core of the HSPG might have little to do with signaling specificity and that the main functional domain of HSPGs is concentrated in the sequence of the heparan sulfate chains.on its protein core. Further mechanisms that allow for differential regulation include processing of HSPGs. These studies suggest a reason for the use of a particular HSPG during an individual developmental decision ?the flexibility of combining both carbohydrate-based regulation and protein-based regulation of cell-cell signaling may make a specific HSPG uniquely suited for a given situation. In the context of combined carbohydrate and protein inputs into HSPG function, it becomes clear that a given HSPG may be expressed and function in very specific contexts that take advantage of its unique regulatory abilities. It is interesting to note that we have connected Perlecan with FGF and Hh signaling in the developing fly brain while mouse studies have shown that Perlecan knock-out mice have cerebral cortex abnormalities [6,19,21]. trol mutant larvae PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28455751 have decreased numbers of circulating hemocytes that are likely due to decreased Ras-MAPK signaling by VEGF/PDGF. Perlecan knock-out mice also have defects in chondrogenesis and cardiovascular development and mammalian studies have demonstrated a role for Perlecan in angiogenesis driven by FGFs, VEGF and PDGF [3]. Finally, we have shown that Perlecan is required for SHH signaling during human prostate cancer growth [8], which reveals a new system for the investigation of the mechanism of Perlecan action. Further analysis of the ability of HSPGs to substitute for each other in cell fate decisions and the means by which they individually regulate cell-cell communication will lead to a clearer understanding of the inputs necessary for cells to carry out a developmental or disease progression.MethodsFly stocks Stocks of the viable trolb22 allele and the lethal trol4, trol7, trol8 and trolsd alleles have been described previously [19,21,22,29]. All trol mutant stocks with the exception of trolb22 are y trolxw/Binsn where the chromosome carrying the trol mutation is marked with y to facilitate identification of y trol mutant versus y+control larvae. The trol-GFP protein trap was obtained from Dr. Stephane Noselli. The bnl06916 and hhAC stocks were obtained from the Bloomington stock center and used to AICAR construct y ; bnl06916/ TM3y+ and y ; hhAC/TM3y+ stocks for genetic studies. PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25534735 Lethal phase Early first instar larvae were collected and placed on apple juice plates with yeast. Each plate initially had 50 mutant or control animals per plate, segregated to prevent competition between mutant and wildtype siblings. Two plates of each genotype were examined. The number and stage of larvae still present on each plate were assayed every 24 hours and the survivors transferred to a fresh plate. Since none of the trol mutants with the exception of trolb22 pro-The carbohydrate-centric view is being challenged by studies that indicate a role for the protein-protein interactions of HSPGs with growth factors and other signaling molecules. For example, expression of chimeric molecules has shown that the cytoplasmic tail of Syndecan is specifically required for FGF2 signaling in addition to its heparan sulfate chains [47]. Perlecan protein-protein interactions include the ability of Perlecan to bind growth factors and extracellu.
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