scholarly journals H Long Terminal Repeat-Associating 2 (HHLA2) is a Biomarker of Advanced Stage Hepatocellular Carcinoma and Promotes Tumor Cell Development In Vitro

2021 ◽  
Vol 27 ◽  
Author(s):  
Min Luo ◽  
Yao Xiong ◽  
Yan Lin ◽  
Rong Liang ◽  
Yongqiang Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Cell ◽  
Long Terminal Repeat ◽  
Cell Development ◽  
Terminal Repeat ◽  
Advanced Stage ◽  
Development In Vitro

Binding of a cellular protein to the gibbon ape leukemia virus enhancer

1987 ◽  
Vol 7 (8) ◽  
pp. 2735-2744
Author(s):  
J P Quinn ◽  
N Holbrook ◽  
D Levens
Keyword(s):  
Long Terminal Repeat ◽  
Specific Binding ◽  
Leukemia Virus ◽  
Cellular Protein ◽  
Terminal Repeat ◽  
Enhancer Activity ◽  
Repeated Element ◽  
Gibbon Ape Leukemia Virus

The gibbon ape leukemia virus (GALV) contains enhancer activity within its long terminal repeat. In the GALV Seato strain this activity resides in a 48-base-pair (bp) repeated element. We demonstrate the existence of a cellular protein which binds in this region of the Seato strain. A sensitive method for enriching protein-DNA complexes from crude extracts coupled with exonuclease and DNase footprint analysis revealed the specific binding of this protein to a 21-bp region within each repeated element. A 22-bp oligonucleotide fragment defined solely by the 21-bp footprint binds a protein in vitro and displays enhancer activity in vivo, suggesting that this protein is a major determinant of GALV enhancer activity. The protein is present in three cell lines which are positive for enhancer activity and is not detected in Jurkat cells, which are negative for enhancer activity. Only GALV long-terminal-repeat variants which support high levels of enhancer activity in vivo compete with this protein for specific binding in vitro, suggesting a potential role for the protein in determining enhancer activity. This protein binding is not inhibited by competition with heterologous retroviral enhancers, demonstrating that it is not a ubiquitous retroviral enhancer binding protein.

Localization of active promoters for eucaryotic RNA polymerase II in the long terminal repeat of avian sarcoma virus DNA

1983 ◽  
Vol 3 (5) ◽  
pp. 811-818
Author(s):  
S A Mitsialis ◽  
J L Manley ◽  
R V Guntaka
Keyword(s):  
Rna Polymerase ◽  
Hela Cell ◽  
Long Terminal Repeat ◽  
Rna Polymerase Ii ◽  
Terminal Repeat ◽  
Avian Sarcoma Virus ◽  
Cell Extracts ◽  
Sarcoma Virus ◽  
Avian Sarcoma

The nucleotide sequences in the long terminal repeat of avian sarcoma virus that are recognized in vitro by HeLa cell RNA polymerase II have been identified. For this purpose, various 5' and 3' deletions were introduced into a cloned long terminal repeat fragment. The effects of these deletions on transcription initiation in HeLa whole-cell extracts were then studied. Three specific transcripts have been identified. The major transcript is initiated at nucleotide +1 (relative to the cap site). Deletion of the upstream sequence between -299 and -55 has no effect on the level of transcription from this start site, whereas deletion of the sequence downstream of -14 drastically reduces the levels of transcription. In contrast, deletion of the sequence downstream from the TATA box has no effect on the initiation or efficiency of synthesis of the two minor RNA species, which are initiated at around nucleotides -260 and -105. The transcription of these RNA products, however, is abolished by an upstream deletion between -299 and -55. These results suggest that HeLa cell RNA polymerase II recognizes in vitro more than one promoter site present in the long terminal repeat of the avian sarcoma virus genome and defines the sequences required for initiation of the major transcript.

Transcriptional activation from the long-terminal repeat of human immunodeficiency virus in Vitro

Virology ◽  
1990 ◽  
Vol 177 (2) ◽  
pp. 606-614 ◽  
Author(s):  
Takashi Okamoto ◽  
Thomas Benter ◽  
Steven F. Josephs ◽  
M. Reza Sadaie ◽  
Flossie Wong-Staal
Keyword(s):  
Human Immunodeficiency Virus ◽  
Long Terminal Repeat ◽  
Transcriptional Activation ◽  
Terminal Repeat ◽  
Immunodeficiency Virus

scholarly journals Localization of active promoters for eucaryotic RNA polymerase II in the long terminal repeat of avian sarcoma virus DNA.

1983 ◽  
Vol 3 (5) ◽  
pp. 811-818 ◽  
Author(s):  
S A Mitsialis ◽  
J L Manley ◽  
R V Guntaka
Keyword(s):  
Rna Polymerase ◽  
Hela Cell ◽  
Long Terminal Repeat ◽  
Rna Polymerase Ii ◽  
Terminal Repeat ◽  
Avian Sarcoma Virus ◽  
Cell Extracts ◽  
Sarcoma Virus ◽  
Avian Sarcoma

The nucleotide sequences in the long terminal repeat of avian sarcoma virus that are recognized in vitro by HeLa cell RNA polymerase II have been identified. For this purpose, various 5' and 3' deletions were introduced into a cloned long terminal repeat fragment. The effects of these deletions on transcription initiation in HeLa whole-cell extracts were then studied. Three specific transcripts have been identified. The major transcript is initiated at nucleotide +1 (relative to the cap site). Deletion of the upstream sequence between -299 and -55 has no effect on the level of transcription from this start site, whereas deletion of the sequence downstream of -14 drastically reduces the levels of transcription. In contrast, deletion of the sequence downstream from the TATA box has no effect on the initiation or efficiency of synthesis of the two minor RNA species, which are initiated at around nucleotides -260 and -105. The transcription of these RNA products, however, is abolished by an upstream deletion between -299 and -55. These results suggest that HeLa cell RNA polymerase II recognizes in vitro more than one promoter site present in the long terminal repeat of the avian sarcoma virus genome and defines the sequences required for initiation of the major transcript.

The long noncoding RNA HOTAIR activates autophagy by upregulating ATG3 and ATG7 in hepatocellular carcinoma

2016 ◽  
Vol 12 (8) ◽  
pp. 2605-2612 ◽  
Author(s):  
Liang Yang ◽  
Xiuwei Zhang ◽  
Hangyu Li ◽  
Jingang Liu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Cell ◽  
Long Noncoding Rna ◽  
Antisense Rna ◽  
Noncoding Rna ◽  
Cell Development

The long noncoding RNA HOX transcript antisense RNA (HOTAIR) has been reported to be an oncogene that influences tumor cell development and that correlates with prognosis in hepatocellular carcinoma (HCC).

ICSBP/IRF-8 retrovirus transduction rescues dendritic cell development in vitro

Blood ◽  
2003 ◽  
Vol 101 (3) ◽  
pp. 961-969 ◽  
Author(s):  
Hideki Tsujimura ◽  
Tomohiko Tamura ◽  
Celine Gongora ◽  
Julio Aliberti ◽  
Caetano Reis e Sousa ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Consensus Sequence ◽  
Myeloid Cell ◽  
Cell Development ◽  
Interleukin 12 ◽  
Final Maturation ◽  
Development In Vitro ◽  
Partner Proteins

Abstract Dendritic cells (DCs) develop from bone marrow (BM) progenitor cells and mature in response to external signals to elicit functions important for innate and adaptive immunity. Interferon consensus sequence binding protein (ICSBP; also called interferon regulatory factor 8 [IRF-8]) is a hematopoietic cell–specific transcription factor expressed in BM progenitor cells that contributes to myeloid cell development. In light of our earlier observation that ICSBP−/− mice lack CD8α+DCs, we investigated the role of ICSBP in DC development in vitro in the presence of Flt3 ligand. Immature ICSBP−/− DCs developed from BM progenitor cells showed assorted defects, did not mature in response to activation signals, and failed to express CD8α and interleukin 12 (IL-12) p40, a feature consistent with ICSBP−/− DCs in vivo. We show that retroviral introduction of ICSBP restores the development of immature DCs that can fully mature on activation signals. All the defects seen with ICSBP−/− DCs were corrected after ICSBP transduction, including the expression of CD8α and IL-12 p40 as well as major histocompatability complex class II and other costimulatory molecules. ICSBP is known to regulate gene expression by interacting with partner proteins PU.1 and IRFs, thereby binding to target elements ISRE and EICE. Analysis of a series of ICSBP mutants showed that the intact DNA-binding activity as well as the ability to interact with partner proteins are required for the restoration of DC development/maturation, pointing to the transcriptional function of ICSBP as a basis of restoration. Taken together, this study identifies ICSBP as a factor critical for both early differentiation and final maturation of DCs.

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