could someone explain the differecne between knockout and knockdown (using RNAi) mice and how they work.?
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Not sure i remember correctly, but i hope it helps.\n\nKnockdown interferes by silencing the gene, as it degrades the expression of a given gene.\n\nKnockout replaces the expression of the gene, producing something else instead.\n\nDon't quote me on it.
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Of course, it's known as the messengerRNA or mRNA. Need morehelp?  I can tell you what happens next.
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There are a number of ways to kill some viruses in eukaryotic cells but usually there are other smarter viruses not affected in the same mechanism.  I will only give a couple of interesting examples.  The first is based on the cellular RNA interference (RNAi) mechanism.  Double strand RNA viruses are processed by an RNase III enzyme into ~20 base pair (bp) long short RNA.  These can bind to mRNA of the virus and lead to their degradation via the RNAi process with Ago2 and the so called RNA induced silencing complex (RISC) mediated pathway.  Some viruses are smart enough to produce a small inhibitor molecule that binds the 20 bp small RNA and thus inhibit the RNAi process.\n\nThere are other processes that target long double stranded RNA - most like from viruses because the cell does not make this type of RNA duplexes.  The recognition of the long dsRNA activate the interferon pathway and lead to apoptosis of the cell and hopefully killing the viruses with it.  However, again there are viruses that produce molecules that inhibit apoptosis and thus will survive long enough to replicate themselves before the cells eventually die.
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While I am a fan of the Cord Blood Registry (the link previously posted), I have to point out that they work with a subset of stem cells, the hematopoietic stem cells, and most of what is talked aobut in the media has to do with embryonic stem cells. Their web site does distinguish the two, but it's worth keeping the difference in mind.\n\nGood link nonetheless.
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Here is the first paragraph of a review article answering your question, see the source below...\n\nLike the discovery of splicing three decades ago, the unearthing of RNA interference (RNAi) and microRNAs (miRNAs) once again has everyone’s attention focused on posttranscriptional phenomena. During RNAi, dsRNA formed in cells by DNA- or RNA-dependent synthesis is processed to ∼20 bp small interfering RNAs (siRNAs) containing 2 nt (nucleotide) 3′ overhangs. These siRNAs are then incorporated into an R NA-i nduced s ilencing c omplex (RISC), which mediates the degradation of mRNAs with high sequence complementarity to the siRNA. MiRNAs are ∼21 nt regulatory RNAs excised from genome-encoded precursors folding into dsRNA-like hairpins. With few exceptions, animal miRNAs base pair imperfectly to the 3′-untranslated region of target mRNAs and inhibit protein accumulation by an unknown mechanism, while plant miRNAs show nearly precise complementarity to their targets and trigger mRNA degradation. This miRNA dualism and observations that miRNAs can act under some circumstances as siRNAs, and vice versa, highlight similarities between the siRNA and miRNA pathways. Indeed, maturation of both RNA classes involves Dicer proteins, and, like siRNAs, miRNAs function as RNP particles, miRNPs or miRISCs, whose composition and, probably, assembly are related to those of the RISC (Sontheimer [2005]; Tomari and Zamore [2005] [ Sontheimer, 2005, Tomari and Zamore, 2005]; consult these reviews when discussed findings are not specifically referenced).
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Saead70 How are you dude! I am teacher at Case Western Reserve University in Cleveland, Ohio and this will help you\n\nWe previously produced three congenic strains carrying lupus susceptibility genes (Sle1-Sle3) from the lupus-prone NZM2410 mouse on the C57BL/6 background and characterized their component phenotypes. Sle1 mediates the loss of tolerance to nuclear antigens; Sle2 lowers the activation threshold of B cells; and Sle3 mediates a dysregulation of CD4+ T cells. We have now created a collection of bi- and tricongenic strains with these intervals and assessed the autoimmune phenotypes they elicit in various combinations. Our results indicate that Sle1 is key for the development of fatal lupus. The combination of Sle1 with Sle2, Sle3, or the BXSB-derived autoimmune accelerating gene yaa results in the development of systemic autoimmunity with variably penetrant severe glomerulonephritis culminating in kidney failure. In contrast, two locus combinations of Sle2, Sle3, and yaa failed to mediate fatal disease. These results indicate that the loss of tolerance to chromatin mediated by Sle1 is essential for disease pathogenesis and identify the pathway occupied by Sle1 as a strategic target for therapeutic intervention in systemic lupus erythematosus. The coexpression of Sle1, Sle2, and Sle3 as a B6-triple congenic results in severe systemic autoimmunity and fully penetrant, fatal glomerulonephritis. These results demonstrate the fulfillment of the genetic equivalent of Koch's postulate, where susceptibility loci in a lupus-prone strain have been identified by a genome scan, isolated and functionally characterized by congenic dissection, and finally shown to mediate full disease expression when recombined in a normal genome.\n\n \nTop \nAbstract \nMaterials and Methods \nResults \nDiscussion \nReferences   \nAlthough the effector mechanisms responsible for the clinical features of systemic lupus erythematosus (SLE) have been studied extensively (1), the primary immunological defects responsible for the initiation and progression of disease remain poorly understood. A wealth of data clearly indicates, however, that genetic predisposition is a key element in susceptibility (2, 3). Several mouse models of lupus displaying different phenotypes and genotypes have collectively contributed a great deal toward our understanding of the disease and have led to the identification of more than 20 genomic intervals associated with susceptibility to SLE or SLE-related phenotypes (4–6). In the NZB/NZW-related NZM2410 lupus-prone strain, we have specifically identified the genomic positions of three recessive loci [Sle1, Sle2, and Sle3 on chromosomes (chr) 1, 4, and 7, respectively] that are strongly associated with SLE-susceptibility (7).\n\nAlthough linkage analyses have provided valuable information about the number and locations of susceptibility genes in lupus-prone strains, they have supplied little information about the nature of the component phenotypes each locus contributes, or how they interact to produce the immunopathology characteristic of the susceptible parental strains. We have adopted a congenic dissection approach to address these issues (8). The basic principle of this approach is to convert a polygenic system into a series of monogenic systems in individual congenic strains, each carrying a single susceptibility interval on a resistant genetic background. The component phenotypes expressed in these strains are amenable to genetic and functional analysis as Mendelian traits. The selection process driving the congenic derivation is purely genetic, i.e., a specific genomic segment is transferred from one strain to another (9). We have produced three congenic strains (10), B6.NZMSle1, B6.NZMSle2, and B6.NZMSle3, by moving each susceptibility interval onto the C57BL/6 (B6) background (Table 1) and used these strains to characterize the primary phenotypes associated with the Sle loci (11). \n\nSle1 mediates the loss of
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I've been reading up on this new research as well. I'm really excited about it and am curious to see how well it works in human trials. Unfortunately, it wouldn't be the first time something looks promising in lab animals but fails miserably in human trials.
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To help elaborate in monkey terms for your reading pleasure , let me explain what these nerds just said.  Once upon a time, Mr cell and Mr. Mito (mitochondria) lived away from each other.  They both had DNA to make more of themselves, but something was wrong  Mr. Cell was having a tough time getting energy and felt weak and miserable because he wanted to grow and divide and be a super cell.  At the same time, Mr. Mito was cold and lonely and needed a place to live where he was safe and where he felt needed and important.  One day Mr Cell accidentally ate Mr mito thinking he was something else.  Mr Mito was angry, but soon came to realize that life was easier inside Mr. Cell because he was protected and could make all the energy he wanted.  Mr. Cell was so happy because he could now use the energy from Mr. Mito to grow strong and become the super cell of his dreams and out live all of the other cell.  They were both happy now and agreed to stay together forever--and they evolved happily ever after.  We will read about Mr.Ribosome and his misfit RNA issues another night.
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I just learned about this a couple of weeks ago, and auto-immune diseases, such as lupus, have a great response to it.  It is called glyco-nutrients.  I don't know how to explain it, other than it is key nutrients, that scientists have discovered that are essential in helping the cells to communicate, so that the body can function properly.  I will put a link to a website that explains the science about it as well as my own website.  You can email me from my website and I will send you more information if you would like.  I was impressed by the science behind it and the results that people were getting.  I hope this helps!
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The latest is a paper that got published in PNAS on transcriptional activation based on dsRNA.  The process is named RNAa for activation in contrast to RNAi for RNA interference.  This process is different from siRNA mediated post-transcriptional gene expression.  \n\nSmall dsRNAs induce transcriptional activation in human cells by Hideki Enokida et al\npnas. 006;103;17337-17342; originally published online Nov 3, 2006; PNAS
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This is a very complex process that forces cells to make commit to an end product while making sure not to allow any redundancies. The genes involved in this process are numerous, but the first to be identified are called the HOX genes. What's interesting about these genes is that they are conserved across a diverse number of species (invertibrates all the way up to mammals).\n\nSo to simplify, the cells of a blastula don't have any idea what they are going to be (face cell, brain cell or liver cell). They have to be told what they are going to be and this is done by the turning on of particular genes which determines the ultimate function of that cell. This selective expression of genes is determined by a complex sequence of events which is dictated by the genes such at teh HOX family of genes. I'm sure there are many other genes and gene families that are involved, but I've given you a couple of sources below that will elaborate. Interestingly, differentiation is a process that not only occurs in multicelllular orgranisms, it also happens in some single-celled organisms (such as the bacterium B. subtilis). I've give you link to the leading researcher in that area also. It may help to understand how things like this happen in its simplest form.
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"Gene therapy is the insertion of genes into an individual's cells and tissues to treat a disease, and hereditary diseases in particular. Gene therapy typically aims to supplement a defective mutant allele with a functional one. Although the technology is still in its infancy, it has been used with some success. Antisense therapy is not strictly a form of gene therapy, but is often lumped together with them."\n\nGo to this site in the source list if should solve the paper your writing... :)
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They both have to do with RNA... I had this on a bio quiz but I forgot...\n\nMRNA: RNA transcribed from the DNA making up a gene. It transmits genetic information from the nucleus to the cytoplasm, where it directs the synthesis of proteins.\n\nTRNA: RNA molecules that carry amino acids to sites on ribosomes where proteins are synthesized.
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Antisense mRNA is an mRNA that is complementary to the coding mRNA.  In cells, an antisense mRNA binds the coding mRNA to produce double-stranded RNA (dsRNA).  This dsRNA is targeted by the cell's RNA interference machinery to downregulate the expression of the original coding mRNA.  This allows a cell to regulate its own genes, which is important in development.
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One is a simple binding assay, in which the ligand (usually radiolabeled) is added to a hemogenate of the tissue-a number of washes are done, in the presence of cold ligand, in order to retain only that ligand that has bound with high affinity.\nThe others are all protein-based.  Western blotting with specific antibodies, immunohistochemistry to determine the presence and cellular localization.  RT-PCR or Northern blotting will tell you if the mRNA is present, but not if the receptor protein itself it there.
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the difference is how they make the cells produce the new genetic material for the viruses. RNA viruses does not require the cells' DNA to reproduce.
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I think they already have something similar to that, don't think it's a pill though. I saw that they were using it a lab mice and they were living like 10 times as long as usual. Something like that anyways. But yes I think they will develop something, might not be in pill form though..