To determine the rather early modifications in gene express

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 To determine the rather early modifications in gene express Empty To determine the rather early modifications in gene express

Post  huwan123456 on Thu Mar 26, 2015 9:29 am

Discussion In recent years numerous members of the classical RASSF family have emerged as vital TSGs. No matter if inactivation of RASSF1 6 [You must be registered and logged in to see this link.] plays a position in leukaemia hasn't however been determined. We discovered that RASSF1 five were not frequently methylated in our series of childhood ALL. Rather, we observed very regular inactivation of RASSF6 reiterating the significance of quite a few classical RASSF mem bers during the development of various kinds of cancer. Evi dence is accumulating that RASSF6 plays a purpose in tumourigenesis and probable functions as being a regulator of apoptosis. RASSF6 is downregulated in 30 60% of a assortment of solid tumours. SiRNA mediated knock down of RASSF6 enhances tumourigenic development in soft agar while RASSF6 overexpression lowers tumour growth in a wide range of tumour cell lines.

The development inhibitory properties [You must be registered and logged in to see this link.] of RASSF6 are probably a result of induction of apoptosis considering the fact that RASSF6 induced cell death was concomitant which has a selection of apoptotic mark ers. Previously, we had demonstrated that RASSF6 interacted with K Ras within a GTP dependent manner and that RASSF6 induced apoptosis was enhanced synergisti cally by co transfection with constitutively active K RasG12V. Thus, RASSF6 can mediate the growth inhibitory properties of Ras proteins. In agreement with earlier research the frequency of mutations to codons twelve, 13 and 61 of each K and N Ras combined in our series of leukaemias was only 14%. Consequently, inactivation of RASSF6 could deliver the choice mech anism of Ras pathway inactivation in B ALL.

In T ALL, in which RASSF6 methylation is less frequent, RASSF1A, RASSF5A and RASSF6 [You must be registered and logged in to see this link.] methylation could account for Ras pathway inactivation in the majority of instances. The lately identified N terminal RASSFs consist of 4 members designated RASSF7 10. RASSF7 ten repre sents a structurally distinct nevertheless evolutionarily conserved sub group on the RASSF loved ones. It's not nonetheless been deter mined whether RASSF7 ten bind to Ras proteins. We found no proof of methylation of RASSF7 in leukae mia cell lines. Hypermethylation with the RASSF8 CpG island and reduction of RASSF8 expression was observed in 2/6 leukaemia cell lines. Nevertheless, considering the fact that we observed RASSF8 CpG island hyper methylation in only 2/19 T ALLs and 4/46 B ALLs we sus pect inactivation of RASSF8 can be concerned while in the pathogenesis of only a modest subset of leukaemias.

RASSF9 was not investigated for inactivation by DNA methylation on account of lack of a CpG island. LOC644943 was quite not too long ago designated RASSF10 based mostly on its homology with RASSF9/P CIP1. The existence of this gene in people has but for being experimentally verified. On the other hand, the Drosophila homologue, CG32150, is expressed in many sensory organ precursors and appears to be necessary for proper Hedgehog pathway signaling. Orthologues of human RASSF10 is usually discovered in several model species like X. laevis and M. musculus. Murine Rassf10 is expressed in several tissues including salivary gland, testes, kidney, lung and brain. X. laevis and M. musculus Rassf10 proteins share 60 and 85% identity with human RASSF10 respectively. To date there has become no investigation of vertebrate RASSF10.

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