What is RISC and how does it help to regulate the expression of genes?
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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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cystic fibrosis transmembrane conductance regulator, or CTRF,gene;it codes for a molecule that acts as a chloride channel.Mutation in it   leads to impaired chloride secretion in airway epithelium. The low level of luminal chloride in the airways (and high levels of sodium) leads to the accumulation of hyper-concentrated, thickened secretions within the respiratory tree.
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It's not really an expression specific to biology\n\nFor example if a car has "all the bells and whistles",  it means that it has all the available options - air conditioning,  power window, cruise control, sound system, etc, including some which might seem a bit ridiculous - fake fur seatcovers, or a horn that plays "Achy Breaky Heart" when it is honked.\n\nSo an artificial chromosome with all the bells and whistles would have every possible gene available crammed into it.
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The only thing I've used it for is to assess whether a target gene was successfully uptaken and expressed in gene transfection, by using a gene that had the GFP gene attached to it.\n\nWikipedia also mentions it being used in the production of biosensors and it is put next to genes in developing organisms to see where and when genes are being expressed.
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cell differentiation \n\nProgressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialised cells, tissues, and organs. When young cells develop as a result of [[cell division, they become differentiated to suit the function they were made for. This is done by the genetic information present in the cell, which will have genes 'switched on' and 'switched off' to determine the function of the cell.
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The above answer pretty much says it...plus, they are under the control of a constitutive promoter, instead of an induced promoter. An induced promoter is that which is induced by the presence of an inducer that binds to the promoter region when there is need for the gene product of the gene that the promoter is controlling. A constitutively expressed gene is one that is expressed everytime the genes of the rest of the genome are expressed. So such a gene product is required in a higher quantity in the body, and that is why it is under the control of a constitutive promoter.
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Genetic engineering, genetic modification (GM), and the now-deprecated gene splicing are terms for the process of manipulating genes, usually outside the organism's normal reproductive process.\n\nIt involves the isolation, manipulation and reintroduction of DNA into cells or model organisms, usually to express a protein. The aim is to introduce new characteristics or attributes physiologically or physically, such as making a crop resistant to a herbicide, introducing a novel trait, or producing a new protein or enzyme. Examples can include the production of human insulin through the use of modified bacteria, the production of erythropoietin in Chinese Hamster Ovary cells, and the production of new types of experimental mice such as the OncoMouse (cancer mouse) for research, through genetic redesign.
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pcr, gene therapy, antisense drugs... umm
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Introduction. This is a brief outline of the steps necessary to produce mice with a mutation targeted to a specific gene. These animals are referred to as "knock-out" mice or "gene targeted" mice. The broad outline of the experiment includes: 1) the investigator constructs a gene targeting vector containing a mutation in the target gene; 2) the targeting vector is introduced into ES cells; 3) ES cell clones which undergo homologous recombination with the targeting vector are identified; 4) ES cell-mouse chimeras are produced; 5) the chimeras breed and transmit the chromosome with the targeted gene to their offspring; 6) homozygous animals are produced from the mating of hemizygous chimera offspring; and 7) the phenotype resulting from the genetic mutation is characterized. Core personnel are available for consultation on all aspects of gene targeting research. Contact Thom Saunders with any questions or Meet the Staff.  The Transgenic Core prioritizes all requests for service on a "first-come, first-serve" basis. Your requests for electroporation, clone expansion, and blastocyst microinjection will be added to the Transgenic Core work queue in the order that they are received. \n2. Plan the experiment. What is the purpose of your experiment? Do you want to completely ablate gene expression in all tissues? Do you want to analyze tissue specific regulatory sequences? Do you want to produce a model for tissue-specific gene deletions? You will need to obtain or clone the structural gene that you want to mutate. The source of the DNA is important since published studies demonstrate genomic DNA isogenic to the embryonic stem cell line give higher gene targeting efficiencies in ES cells (see Key Gene Targeting Papers). While complete sequence information is not necessary, a detailed restriction map of the gene is an irreplaceable tool. During the planning stages the material transfer agreements for R1 ES cells and other reagents should be initiated so that they are ready in time. Once a genomic clone of the gene is in hand and restriction mapped, then it is time to... \n\n3. Clone and the Verify the Targeting Vector. The Core has cloning vectors for investigators to use in gene targeting research. They include pPNT, a basic targeting vector, pNZTK2, designed to insert the lacZ gene behind the promoter of the targeted gene, and pflox, which is designed to introduce loxP sites into the gene. A complete materials transfer agreement is required before they can be distributed. You will need to determine which 5' and 3' fragments of the gene will be used to construct the targeting vector. Generally speaking, a couple of Kb on either end should give a reasonable gene targeting frequency. You will also need to consider the methods and probes that you will use to identify ES cell clones that have undergone homologous recombination with the targeting vector. This means a Southern blot approach with probes outside of the targeting vector or a PCR based assay with primers outside of the targeting vector. Once the orientation of the fragments in the targeting vector are confirmed and the probes are tested then it is time to... \n\n4. Electroporate ES Cells and Select Recombinants. ES cells are a very sensitive reagent, and most often the weakest link in the process of producing gene targeted mice. Fastidious tissue culture technique is necessary to maintain the totipotent state of the cells during electroporation, selection, and expansion. In order to maximize successful outcomes, the Transgenic Core maintains ES cells and companion reagents that are quality tested by producing ES cell-mouse chimeras that transmit the ES cell genome to offspring. Investigators may choose to use the Core's Gene Targeting Service (we do all of the tissue culture work, you do all of the molecular biology), or to use space in the Core lab (rent space in our completely equipped laboratory for ES cell culture work), or to do th
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Hmmm. I think your interpretation is skewed. Apoptosis (programmed cell death) is a mechanism to prevent further growth (not death). Eventually, anything that stops to grow wears down (and dies). Our bodies continue to produce many new cells throughout our lifetime (ex. skin cells) but some (ex. nerve and muscle tissue of the heart) are not produced again after they 'die' (hence stem cell research). Oh, to tie that back in to your original question, DNA does control apoptosis... however, when those genes containing that DNA malfunction (as in many types of cancer), cells may continue to grow and divide (to produce more cells) which then form tumors -- so, I personally hope that this mechanism doesn't change!
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1. Usually all living cells of the same organism have the same exact DNA. But the cell type determines which genes are actually expressed.\n\n2. Eukaryote are more complex cells and have a longer time between transcription and a a functional protein. They use repression, signal cascades, phosphorylation, etc. A prokaryote has simpler regulation because transcription itself is usually the regulation.\n\n3. Vertebrates have 4 groups of hox genes, fruit flies only have one group. Look at the way the hox genes are expressed in development and what specifically they do (Sorry I can't give a more direct answer, I don't remember enough of my animal biology.)\n\n4. Polyploidy generally makes plants bigger, this makes their fruit bigger also. Another advantage is manipulation of fertilization. For example: seedless watermelon is produced by crossing a diploid with a tetraploid to get an infertile triploid. The embryos abort in the triploid and fail to form mature seeds.
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"silent information regulator" proteins.
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Learn assembler\n\nuse softice or linice to read memory changes\n\n\nsee what changes what and where then make a proggy to manipulate values in the memory.
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Now-a-days, not much.  RISC used to be faster because it used simpler rules to process information in the CPU.  But today processors are so fast that the complex instructions of CISC are usually more efficent.  It depends on the device that the CPU is in though.  But the theory was that it was faster to process 4 instuctions that that took 1 clock cycle each than to process one instruction that took 8 clock cycles.  You really get down into low level computer engineering with CISC and RISC.  But here's a simple example of how they work.  In RISC to multiply 2 times 4 the CPU would call an addition instruction and do it 4 times.  In other words to get the answer the CPU would add 2 + 2 + 2 + 2 to get 8.  In CISC there would be a multiplication instruction in the CPU and it would simply take 2 and multiply it by 4 based on how this instruction told it to.  But the problem is that while an addition instruction might only take 1 clock cycle to perform, the multiplication instruction might take 8.  It gets more complex than that, but I hope that gives you an idea.  This is also all happening in binary so you can look up how to multiply binary numbers and you'll see why it can get complex.
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Software \nBayesian Analysis of Gene Expression Levels (BAGEL): a program for the statistical analysis of spotted microarray data.
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They keep a record of who you are, and pass on that record to your offspring.  DNA, which is contained in your chromosomes, is the program to create a human being.  The program is rewritten every time a new person is created, but the subroutines, if you will, come from their parents.  Useful if you want to continue the human race!
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proto-oncogenes are genes that normally function in regulating proliferation. Mutations that activate them will usually cause the cell to growth without control (this is when we refer to them as oncogenes).\nTumor suppressor genes are caretakers and gatekeepers. They make sure to control uncontrolled proliferation and give the time to a cell to repair any damage. If necessary, wil cause the cell to die. If these genes get mutated then cells would tend to keep unrepaired DNA damages and turn into tumors.