cloning!

There are many social challenges a cloned child might face in my opinion. One major challenge is the fact the child doesn't have real blood related parents so the child may feel all alone. Another challenge is having to be constantly watched and studied by scientists. Therefore the child may not have privacy or be able to do the normal things a child experiences in their life. Also if people find out the child isn't human they may be scared or bully the child saying the child is a alien.

extra credit

The first semester of biology was very fun i made a lot of new friends. I was confused and struggled a bit in class but I'm starting to get used to the curriculum. I was somewhat confused in each topic but i got the hang of it because when i think back i actually learned a lot. My strong point in biology is anything that has to do with medical things because I understand it and when I'm older i would like to be in the medical field. My favorite lab was the sex virus one because everyone in class was running around saying funny jokes involving the lab. My least favorite experiment was when we had to use the microscope because i didn't know what to look for or if i found it. One thing i think would make the class better is if the notes and homework were on power points because its easier to take notes and to do the homework in my opinion.

transcription and translation

In transcription there are 5 steps. The 1st step is the helix unzips. The 2nd step is the promoter attaches. The 3rd step is the beginning of RNA synthesis. The 4th step is it makes a compliment starting at the promoter. The 5th step is DNA zips back up. The 5 steps of translation are 1.amino acids attach to the tRNA 2.tRNA transfers to ribosomes 3.tRNA attaches to mRNA 4.tRNA comes and repeats 5.DNA continues to transfer until it sees UAA which is a stop codon

gene sequences

GENE SEQUENCE 1.Huntingtin is a disease gene linked to Huntington's disease, a neurodegenerative disorder characterized by loss of striatal neurons. This is thought to be caused by an expanded, unstable trinucleotide repeat in the huntingtin gene, which translates as a polyglutamine repeat in the protein product. A fairly broad range in the number of trinucleotide repeats has been identified in normal controls, and repeat numbers in excess of 40 have been described as pathological. The huntingtin locus is large, spanning 180 kb and consisting of 67 exons. The huntingtin gene is widely expressed and is required for normal development. It is expressed as 2 alternatively polyadenylated forms displaying different relative abundance in various fetal and adult tissues. The larger transcript is approximately 13.7 kb and is expressed predominantly in adult and fetal brain whereas the smaller transcript of approximately 10.3 kb is more widely expressed. The genetic defect leading to Huntington's disease may not necessarily eliminate transcription, but may confer a new property on the mRNA or alter the function of the protein. One candidate is the huntingtin-associated protein-1, highly expressed in brain, which has increased affinity for huntingtin protein with expanded polyglutamine repeats. This gene contains an upstream open reading frame in the 5' UTR that inhibits expression of the huntingtin gene product through translational repression. [provided by RefSeq, Jul 2008]
GENE SEQUENCE 2.his gene encodes a protein that is one of the two components of elastic fibers. The encoded protein is rich in hydrophobic amino acids such as glycine and proline, which form mobile hydrophobic regions bounded by crosslinks between lysine residues. Deletions and mutations in this gene are associated with supravalvular aortic stenosis (SVAS) and autosomal dominant cutis laxa. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
GENE SEQUENCE 3.Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1 or PSEN2) or the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor such that, they either directly regulate gamma-secretase activity, or themselves act are protease enzymes. Two alternatively spliced transcript variants encoding different isoforms of PSEN2 have been identified. [provided by RefSeq, Jul 2008]
GENE SEQUENCE 4.CD133 depletion effect on metastatic melanoma cell line, Expression profiling by array, transformed count
GENE SEQUENCE 5.This gene encodes a member of the fibrillin family. The encoded protein is a large, extracellular matrix glycoprotein that serve as a structural component of 10-12 nm calcium-binding microfibrils. These microfibrils provide force bearing structural support in elastic and nonelastic connective tissue throughout the body. Mutations in this gene are associated with Marfan syndrome, isolated ectopia lentis, autosomal dominant Weill-Marchesani syndrome, MASS syndrome, and Shprintzen-Goldberg craniosynostosis syndrome. [provided by RefSeq, Jul 2008]
GENE SEQUENCE 6.The protein encoded by this gene is a negative regulator of the cell cycle and was the first tumor suppressor gene found. The encoded protein also stabilizes constitutive heterochromatin to maintain the overall chromatin structure. The active, hypophosphorylated form of the protein binds transcription factor E2F1. Defects in this gene are a cause of childhood cancer retinoblastoma (RB), bladder cancer, and osteogenic sarcoma. [provided by RefSeq, Jul 2008]