DNA-binding domain

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    nucleocapsid (NC), p6 domains, and two spacer peptides, SP1 and SP2. Each of these HIV-1 structural proteins play a crucial role in the HIV-1 retroviral replication cycle. MA is responsible for targeting Gag to the plasma membrane and promoting the incorporation of viral envelop glycoproteins into the forming virions; CA drives Gag multimerization during assembly to form the Gag lattice that encapsidates the viral RNA genome; NC recruits the viral RNA genome into the virions; and the p6 domain recruits the

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    Lab Report

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    might be an important event of PPARγ in epithelial cells along with its anti-inflammatory activities. To investigate the basis for Muc5AC repression by PPARγ, we analyzed the MUC5AC promoter for the presence of putative PPARγ transcription factor binding elements that may mediate this response. As shown in schematic representation, our analysis identified a novel PPARγ response elements (PPRE) between -3834 and -3821 bp (PPRE1: TGTTCAGAGGTCAA) and between -1207 and -1194 bp (PPRE2: AGGACAAAGGGCC)

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    Being able to determine the amount of DNA present in an organism has been successfully done using qPCR. In this experiment, qPCR was used to identify how much fungi could infect mutant and wildtype lines of A. thaliana. Also, qPCR was used to amplify the 16s rRNA ITS (internal transcribed spacer) of an unknown fungal pathogen. Other ways qPCR has been used in recent years include the use of qPCR to quantify copy number variants in the HER-2 gene which is a proto-oncogene. This method was particularly

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    IgG monoclonal antibody that binds to the HER2. Antitumor activity of trastuzumab has not been discovered entirely, but, it is assumed to result in antibody dependent cell mediated cytotoxicity, declined intracellular signal transduction, decreased DNA repair and anti angiogenic effects(7). Trastuzumab based treatment policy has established a landmark in the

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    De Lean and Lefkowitz carried out competitive binding experiments to investigate the interaction between extracellular ligands (both antagonist and agonist), GPCRs and X - a membrane component. Method The antagonist [3H]DHA and the agonist [3H]HBI were incubated with freshly prepared plasma membranes

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    key developmental genes, such as homeotic genes. PcG proteins maintain silent states of gene expression, while the trxG of genes counteracts silencing with a chromatin opening function. In Drosophila, PcG and trxG complexes are recruited to specific DNA elements named as PcG and trxG response elements (PREs and TREs, respectively). Once recruited, these complexes seem to be able to establish silent or open chromatin states that can be inherited through multiple cell divisions even after decay of the

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    fuse with the host cell. Preventing the entry of HIV into CD4 cells has lead to the development of a new type of antiretroviral drugs (ARV’s) called entry inhibitors. Maraviroc is a CCR5 receptor antagonists; this prevents the HIV Gp120 protein from binding and infecting the host

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    CCR1 Case Study

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    tendency for HIV-1 to select CCR5 co receptors for attachment and fusion promoted the development of CCR5 antagonists. A 32bp deletion in the CCR5 gene which creates a truncated receptor was discovered in Caucasian populations in 1996. After assessing DNA from individuals given through various families and by anonymous donors through the genetics department at the Erasme hospital in Brussels, scientist concluded roughly ~10% of people in the population contained this mutant allele. This 32bp deletion

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    the function of these regions within the genome, they must first be identified. After determining the conserved sequences, they can then be classified according to function. One particularly informative way to decipher the function of a non-coding DNA sequence is to determine

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    way that they lack cell wall and cell membrane. They contain a core of nucleic acid that may be DNA or RNA, surrounded by the protein coat. Viruses are obligate intracellular parasites, which means that they cannot grow outside the host cell, they always require a host cell for their multiplication. They use the host machinery for its multiplication. They can

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