how does photo-oncogene and tumor-suppressor genes work in a cell ?how do they tie in with DNA replication?
493151
its proto-oncogene, read here\n\nhttp://en.wikipedia.org/wiki/Tumour_suppressor_gene\n\nhttp://en.wikipedia.org/wiki/Proto-oncogene
625682
cromosomes are the hereditary stuffs n d cell.they r segments of dna. mitosis is equational division taking place in somatic or germ celll ( i.e not reproductive)\n\nso d hereditary matter or d gene in alll cells of an organism remains same. so for mitosis chromosomes are very important.\nin dis process,,,, chromosomes replicate and divide themslves resulting in karyokinesis(splittng of nucleus ) followed by cariocynesis ( sdividing of d cells_\n\n\n\nCHROMOSOMES carry most of the genetic material and therefore they:\n\ncarry inherited traits \ncarry the organisation of the cell life \nheredity: each pair of homologues consists of one paternal and one maternal chromosome --> diploidy (2 lots). The intact set is passed to each daughter cell at every mitosis. \ncell life: will be perturbed if regular segregation fails \n\nduring embryogenesis (constitutional anomalies). \nin a cancer (acquired anomalies).
766661
do you mean what processes cells must undergo? \n\nIf that's your question, then the processes would be cell division by mitosis (to produce more cells, so that organism can increase in size/length), cell elongation(this occurs mainly in plants via vacuolation and thus aids in increase in size and length) and cell differentiation(this allows genes to be switched on or off so that certain traits/phenotypes can be expressed, eg. gene that codes for blue eyes switched on for cell in the eye and not elsewhere like cell on the hand/feet). Hope this answers your question.
20677
That's a great question. There's a whole field called developmental biology that researches how organisms develop from single cells into complex organisms. The short answer is that different genes get turned on and turned off at the right times, and this causes cells to divide, move, differentiate (turn into different kinds of cells) and make connections with other cells. A lot of work has been done and a lot of work is still being done on figuring out exactly what the signals are that make this happen in an organized way.\n\nAn important reason that a lot of people work on this, in addition to understanding our world and ourselves better, is that the genes that work during development are often the genes that get messed up in cancer and other diseases. By understanding their normal role, we can better understand what happens when they aren't working right.
906596
Post Replication Repair Mechanism - DNA Repair\n\nThe reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions.  The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strands; photo reactivation repair, in which the lethal and mutagen effects of ultraviolet light are eliminated; and post -replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex.  Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
286735
DNA is what makes up our genes.  It is several long chains (polymers) of molecules that contain a 'chemical code' that the body uses to make proteins (proteins are many types of molecules that are necessary for the body to make and run itself).  These long chains of DNA are grouped into 23 different chromosomes.  You have two pairs of each chromosome - one set of 23 from your mom and the other set of 23 from your dad.  So, in total, you have 46 chromosomes in each cell.\n\nEach cell in your body has the same DNA.  But a liver cell is different from a skin cell, etc.  That is because each cell type has access to only certain genes in your DNA (to make the proteins needed specifically for that type of cell).\n\nStructurally, DNA looks like a flexible ladder (like a rope ladder).  The runs of the ladder (the sides) are the long chains or polymers and consist of a sugar group connected to a phosphate group, connected to the next sugar group, and so on.  Between these side chains are pairs of 'bases' - Adenine, Thymine, Guanine, and Cytosine (A T G  C).  These are the actual code that contains the information in your genes.\n\nThe 'ladder' of DNA twists around itself to form a shape called a 'double helix'.\n\nI hope this is helpful to you.  Good luck!
1011098
we have cells.cells contain nucleus.nucleus has chromayin network.chromatin network is actually  chromosomes.chromosomes have  genes located on them at specific places called locus.these genes nothing but nucleotide sequences that determine our various characters like height,weight,eye colour etc.they contain codes for specific proteins in our body.any damage to it in the form of mutation we are affected by terriblre diseases.thats the long and short of it.
494983
Do you mean proto-oncogene?\nhttp://en.wikipedia.org/wiki/oncogene#pr...\n\nhttp://en.wikipedia.org/wiki/tumor_supre...
337914
Ultraviolet light is able penetrate through the outer cells of our integument (skin). Doing this exposes the DNA to potential damage. \n\nThe damage that is proposed to be caused by the UV light has changed in recent years. It used to be thought that UV light caused the base pairs to fuse (a base pair refers to the fact that complimentary bases from opposite strands hydrogen bond with one another -- Adenine (A) bonds with Thymine (T); Guanine (G) pairs with Cytosines (C). Howver, it's been recently shown that as sunlight warms our skin, UV photons are absorbed by the bases, causing their electrons to vibrate. These high-energy vibrations nudge the atoms in the bases around. If all goes well, the DNA returns to normal after the energy wave passes. But some of the time, the atoms don't return to their original positions, and new chemical bonds are formed.\n\nScientists know that such accidental bonds create "photolesions" - injuries that prevent DNA from replicating properly. The details of the process aren't fully understood, but studies suggest that photolesions cause genetic mutations that lead to diseases such as sun damage as well as cancer.\n\nBecause skin cells need to replicate often this damage can either slow them down causing skin damage or speed them up to the point of becoming cancerous.
767384
Most of the cells in your body are identical in terms of genetic content (DNA/chromosomes).\n\nThe huge variety of cells is due to the fact that as we develop from a fertilized egg into an embryo and beyond, there are different signals passed around constantly that direct cells to divide and grow in certain ways such that a human being is the end result.  Throughout life, these "molecular instructions" are maintained so that our cells stay the proper type.  (Sometimes, improper maintenance of these directions can lead to cancer.)\n\nExpression of genes (that is, transcription from DNA to mRNA, and then translation to protein) will of course dictate how the process goes.  Different proteins exist in each different cell type due to variable expression.
507551
For any kind of cancer it has to do with the cells, now each cell has a copy of DNA, but it duplicates this in the form of RNA and sends that arround the cell to do the going ons.  However cancer results when a certain part of the RNA is miss duplicated, this dosn;t happen very often respectivley since there is somthing that goes over the RNA to make sure it is correct.  However when that substance has a problem it cannot check the RNA and therefore cancer is much more likley.  Because cancer is the rapid reproduction of cells and when the RNA dosn't tell the cell to stop reproducing it makes more and more cells.  Things like ciggarets destroy the substance making them much more likley to get cancer.  So ya thats just a really breif crash course, i reckon you google it if you have anymore questions.
852458
there is a tumour suppressor gene that mutates and dont work. the new cell growth just keeps going there is no stop
448280
DNA from organisms displaying both normal and abnormal phenotypes. Mutation studies can be done, comparing the sequences of normal and abnormal, isolating the gene in question and identifying the protein it encodes. "Knock-out" experiments can also be done, wherein the effect of deleted genes will be observed. Other things to consider would be promoters, suppressors and regulators of the gene.
558764
Cancer, in laymans's terms, is the unregulated growth of a cell.  Now cell growth, and activities in general, are typically regulated through cell receptors which, in response to a stimulus, activate or release a kinase.  These kinases transfers phosphates to other proteins or phosphorylates them making them active to stimulate DNA replication and transcription (growth).  Cancer is commonly characterized by high levels of (active) kinase due to suppressed phosphotase activity (opposite of a kinase) or defective oncoreceptors stuck in the "ON" position.
373524
well,\n*CGH:is a molecular-cytogenetic method for the analysis of copy number changes( gains/losses)in the DNA content of tumor cells,method is based on the hybridization of fluorescently labeled tumor and normal DNA to normal human metaphase preparations,using epiflourescence microscopy and quantitative image analysis,regional differences in the fluorescence ratio of tumor vs.control DNA can be detected and used for identifying abnormal regions in the tumor cell genome,CGH will detect only unbalanced chromosomes changes,structural chromosome aberrations such as balanced reciprocal translocations,inversions can not be detected.
403858
It's pretty well established that the apoptotic machinery gets deprogrammed by cells progessing through tumorogenesis.  One way is the well understood p53/Mdm2 pathway.  P53 is a tumor supressor and, upon DNA damage, can either halt cells to repair the damage (at the G1/S checkpoint) or trigger apoptosis.  It does this by promoting gene expression.  \n\nAnother mechanism is to inhibit t-cell induced apoptosis, by deregulation of FasL and other proteins.\n\nThere's a whole bunch of info in the Cancer Medicine book online at NCBI (below).
484734
I think you mean "mitogen".  A mitogen is a chemical that will induce living cells to replicate themselves via the mitotic cell division process.  Many types of cells are prompted to begin the division process by naturally occurring mitogens, usually proteins, often referred to as growth factors or cytokines.  Such proteins initiate a second-messenger signal transduction pathway called the mitogen-activated protein kinase (MAPK) mechanism that ultimately triggers mitosis in the target cell.\n\nMitogens are also used in the laboratory to create colonies of identical cells, beginning with one or many cells having specific origin and characteristics.  For example, they are used in experimental immunology to produce clones of T- or B-lymphocytes and other leukocytes capable of mounting an immune response to a specific antigen of interest, or expressing cell membrane surface markers (HLA antigens) of interest.  The two I am most familiar with are pokeweed mitogen and concanavalin-A, both of which are derived from plants.