WordNet

relating to or occurring in a term or fixed period of time; "terminal examinations"; "terminal payments"
a contact on an electrical device (such as a battery) at which electric current enters or leaves (同)pole
station where transport vehicles load or unload passengers or goods (同)terminus, depot
electronic equipment consisting of a device providing access to a computer; has a keyboard and display
being or situated at an end; "the endmost pillar"; "terminal buds on a branch"; "a terminal station"; "the terminal syllable"
causing or ending in or approaching death; "a terminal patient"; "terminal cancer"
of or relating to or situated at the ends of a delivery route; "freight pickup is a terminal service"; "terminal charges"
do over; "They would like to take it over again" (同)take_over
an event that repeats; "the events today were a repeat of yesterdays" (同)repetition
to say again or imitate; "followers echoing the cries of their leaders" (同)echo
to say, state, or perform again; "She kept reiterating her request" (同)reiterate, ingeminate, iterate, restate, retell

PrepTutorEJDIC

『終りの』,末端の / 毎期の,定期の;学期末の / 『死に至る』, / 末端 / (電池の)端子 / (町の中心に近い)空港バス発着場;(一般に,鉄道・バスの)終点,終着駅
〈自分がすでに一度言ったこと)‘を'『繰り返して言う』 / 〈他人の言ったこと〉‘を'おうむ返しに言う;…‘を'他の人に繰り返して言う / …‘を'『暗記して言う』,暗唱する / …‘を'繰り返して行う(do again) / (食べたあとで)〈食物の〉味が残る / 〈小数が〉循環する / 繰り返すこと,反復すること / 繰り返されるもの,(公演の)再演;(番組の)再放送 / 反復楽節;反復記号(∥: :∥)
繰り返して言われる(行われる)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/03/15 01:40:11」(JST)

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Long terminal repeats (LTRs) are identical sequences of DNA that repeat hundreds or thousands of times found at either end of retrotransposons or proviral DNA formed by reverse transcription of retroviral RNA. They are used by viruses to insert their genetic material into the host genomes.

The HIV-1 LTR is approximately 640 bp in length and, like other retroviral LTRs, is segmented into the U3, R, and U5 regions. U3 and U5 has been further subdivided according to transcription factor sites and their impact on LTR activity and viral gene expression. The multi-step process of reverse transcription results in the placement of two identical LTRs, each consisting of a U3, R, and U5 region, at either end of the proviral DNA. The ends of the LTRs subsequently participate in integration of the provirus into the host genome. Once the provirus has been integrated, the LTR on the 5′ end serves as the promoter for the entire retroviral genome, while the LTR at the 3′ end provides for nascent viral RNA polyadenylation and, in HIV-1, HIV-2, and SIV, encodes the accessory protein, Nef.^[1]

All of the required signals for gene expression are found in the LTRs: Enhancer, promoter (can have both transcriptional enhancers or regulatory elements), transcription initiation (such as capping), transcription terminator and polyadenylation signal.^[2]

In HIV-1, the U5 region has been characterized according to functional and structural differences into several sub-regions as follows:

TAR or trans-acting responsive element, plays a critical role in transcriptional activation via its interaction with viral proteins. It forms a highly stable stem-loop structure consisting of 26 base pairs with a bulge secondary structure that interfaces with the viral transcription activator protein Tat.^[3]

Poly A play roles both in dimerization and genome packaging since it is necessary for cleavage and polyadenilation. It has been reported that sequences upstream (U3 region) and downstream (U5 region) are needed in order to make the cleavage process efficient.^[4]

PBS or primer binding site, of 18 nucleotides long, it has a specific sequence that bind to tRNALys and are requirements for initiation of reverse transcription.^[5]

Psi (Ψ) or the packaging signal is a unique motif that is associated with this process, although is not sufficient to specify for packaging. It is composed of four stem-loop (SL) structures with a major splicing donor site embedded in the second SL.^[6]

DIS or dimer initiation site that mediates RNA-RNA interactions. Is a highly conserved stem-loop sequence found in many retroviruses and is characterized by a conserved stem and palindromic loop, when homodimerized, forms a “kissing-loop” complex.^[7]

The transcript begins, by definition, at the beginning of R, is capped, and proceeds through U5 and the rest of the provirus, usually terminating by the addition of a poly A tract just after the R sequence in the 3' LTR.

The finding that both HIV LTRs can function as transcriptional promoters is not surprising since both elements are apparently identical in nucleotide sequence. Instead, the 3' LTR acts in transcription termination and polyadenylation. However, it has been suggested that the transcriptional activity of the 5' LTR is far greater than that of the 3' LTR, a situation that is very similar to that of other retroviruses.^[2]

During transcription of the human immunodeficiency virus type 1 provirus, polyadenylation signals present in the 5' long terminal repeat (LTR) are disregarded while the identical polyadenylation signals present in the 3'LTR are utilized efficiently. It has been suggested that transcribed sequences present within the HIV-1 LTR U3 region act in cis to enhance polyadenylation within the 3' LTR.^[8]

Transcription[edit]

The LTRs are partially transcribed into an RNA intermediate, followed by reverse transcription into complementary DNA (cDNA) and ultimately dsDNA (double-stranded DNA) with full LTRs. The LTRs then mediate integration of the retroviral DNA via an LTR specific integrase into another region of the host chromosome. The first LTR sequences were derived by A.P. Czernilofsky and J. Shine in 1977 and 1980.^[9]^[10]

Retroviruses such as Human Immunodeficiency Virus (HIV) use this basic mechanism.

Dating retroviral insertions using LTRs[edit]

As 5' and 3' LTRs are identical upon insertion, the difference between paired LTRs can be used to estimate the age of ancient retroviral insertions. This method of dating is used by paleovirologists, though it fails to take into account confounding factors such as gene-conversion and homologous recombination.

External links[edit]

Long Terminal Repeat at the US National Library of Medicine Medical Subject Headings (MeSH)

References[edit]

^ Krebs, Fred C.; Hogan, Tricia H.; Quiterio, Shane; Gartner, Suzanne; Wigdahl, Brian (2001). "Lentiviral LTR-directed Expression, Sequence Variation, and Disease Pathogenesis". In Kuiken, C; Foley, B; B; Marx, P; McCutchan, F; Mellors, JW; Wolinsky, S; Korber, B. HIV Sequence Compendium 2001. Los Alamos, NM: Theoretical Biology and Biophysics Group, Los Alamos National Laboratory. pp. 29–70.
^ ^a ^b Klaver, B; Berkhout, B (1994). "Comparison of 5' and 3' long terminal repeat promoter function in human immunodeficiency virus". Journal of virology 68 (6): 3830–40. PMC 236888. PMID 8189520.
^ Wu, Yuntao (2004). "HIV-1 gene expression: Lessons from provirus and non-integrated DNA". Retrovirology 1: 13. doi:10.1186/1742-4690-1-13. PMC 449739. PMID 15219234.
^ Valsamakis, A; Schek, N; Alwine, JC (1992). "Elements upstream of the AAUAAA within the human immunodeficiency virus polyadenylation signal are required for efficient polyadenylation in vitro". Molecular and cellular biology 12 (9): 3699–705. PMC 360226. PMID 1508176.
^ Goldschmidt, V.; Rigourd, M; Ehresmann, C; Le Grice, SF; Ehresmann, B; Marquet, R (2002). "Direct and Indirect Contributions of RNA Secondary Structure Elements to the Initiation of HIV-1 Reverse Transcription". Journal of Biological Chemistry 277 (45): 43233–42. doi:10.1074/jbc.M205295200. PMID 12194974.
^ Johnson, Silas F.; Telesnitsky, Alice (2010). "Retroviral RNA Dimerization and Packaging: The What, How, when, Where, and Why". In Madhani, Hiten D. PLoS Pathogens 6 (10): e1001007. doi:10.1371/journal.ppat.1001007. PMC 2951377. PMID 20949075.
^ Heng, Xiao; Kharytonchyk, Siarhei; Garcia, Eric L.; Lu, Kun; Divakaruni, Sai Sachin; Lacotti, Courtney; Edme, Kedy; Telesnitsky, Alice et al. (2012). "Identification of a Minimal Region of the HIV-1 5′-Leader Required for RNA Dimerization, NC Binding, and Packaging". Journal of Molecular Biology 417 (3): 224–39. doi:10.1016/j.jmb.2012.01.033. PMC 3296369. PMID 22306406. |displayauthors= suggested (help)
^ Brown, PH; Tiley, LS; Cullen, BR (1991). "Efficient polyadenylation within the human immunodeficiency virus type 1 long terminal repeat requires flanking U3-specific sequences". Journal of virology 65 (6): 3340–3. PMC 240993. PMID 1851882.
^ Shine, J.; Czernilofsky, A. P.; Friedrich, R.; Bishop, J. M.; Goodman, H. M. (1977). "Nucleotide sequence at the 5' terminus of the avian sarcoma virus genome". Proceedings of the National Academy of Sciences 74 (4): 1473–7. doi:10.1073/pnas.74.4.1473. PMC 430805. PMID 67601.
^ Czernilofsky, A.P.; Delorbe, W.; Swanstrom, R.; Varmus, H.E.; Bishop, J.M.; Tischer, E.; Goodman, H.M. (1980). "The nucleotide sequence of an untranslated but conserved domain at the 3′ end of the avian sarcoma virus genome". Nucleic Acids Research 8 (13): 2967–84. doi:10.1093/nar/8.13.2967. PMC 324138. PMID 6253899.

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English Journal

1H, 13C and 15N assignments of Sgt2 N-terminal dimerisation domain and its binding partner, Get5 Ubiquitin-like domain.

Simon AC, Simpson PJ, Hawthorne W, Hale LR, Goldstone RM, Isaacson RL.SourceDivision of Molecular Biosciences, Imperial College London, Exhibition Road, South Kensington, London, SW7 2AZ, UK.
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The first stage of the GET (guided entry of tail-anchored proteins) mechanism for tail-anchored (TA) membrane protein insertion is thought to occur when Sgt2 (small, glutamine-rich, tetratricopeptide repeat-containing protein 2) binds TA proteins upon their release from the ribosome. It sorts them a
PMID 23001946

Annexin A1 is regulated by domains cross-talk through post-translational phosphorylation and SUMOYlation.

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A role of mitochondrial complex II defects in genetic models of Huntington's disease expressing N-terminal fragments of mutant huntingtin.

Damiano M, Diguet E, Malgorn C, D'Aurelio M, Galvan L, Petit F, Benhaim L, Guillermier M, Houitte D, Dufour N, Hantraye P, Canals JM, Alberch J, Delzescaux T, Déglon N, Beal MF, Brouillet E.SourceThe first two authors contributed equally to the present study.
Human molecular genetics.Hum Mol Genet.2013 Oct 1;22(19):3869-82. doi: 10.1093/hmg/ddt242. Epub 2013 May 29.
Huntington's disease (HD) is a neurodegenerative disorder caused by an abnormal expansion of a CAG repeat encoding a polyglutamine tract in the huntingtin (Htt) protein. The mutation leads to neuronal death through mechanisms which are still unknown. One hypothesis is that mitochondrial defects may
PMID 23720495

Japanese Journal

A high excision potential of TALENs for integrated DNA of HIV-based lentiviral vector.

Ebina Hirotaka,Kanemura Yuka,Misawa Naoko,Sakuma Tetsushi,Kobayashi Tomoko,Yamamoto Takashi,Koyanagi Yoshio
PLOS ONE 10(3), 2015-03-17
… We recently reported that HIV proviral DNA could be excised from the chromosomal DNA of HIV-based lentiviral DNA-transduced T cells after multiple introductions of a clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 endonuclease system targeting HIV long terminal repeats (LTR). …
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Quantitative analysis of APP axonal transport in neurons: role of JIP1 in enhanced APP anterograde transport

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Efficient screening of long terminal repeat retrotransposons that show high insertion polymorphism via high-throughput sequencing of the primer binding site

Monden Yuki,Fujii Nobuyuki,Yamaguchi Kentaro,Ikeo Kazuho,Nakazawa Yoshiko,Waki Takamitsu,Hirashima Keita,Uchimura Yosuke,Tahara Makoto
Genome 57(5), 245-252, 2014-06-25
… Although a large number of long terminal repeat (LTR) retrotransposon families exist in the higher eukaryotic genomes, the identification of families that show high insertion polymorphism has been challenging. …
NAID 120005468263