The first intron of the human α2(I) collagen gene (COL1A2) contains a novel interferon-γ responsive element

2007 ◽  
Vol 26 (3) ◽  
pp. 185-189 ◽  
Author(s):  
Shizuko Tanaka ◽  
Francesco Ramirez
Keyword(s):  
Interferon Γ ◽  
Collagen Gene ◽  
First Intron ◽  
Responsive Element

scholarly journals Identification of an enhancer sequence within the first intron required for cartilage-specific transcription of the α2(XI) collagen gene. VOLUME 275 (2000) PAGES 12712-12718

2009 ◽  
Vol 284 (17) ◽  
pp. 11748.2-11748 ◽  
Author(s):  
Ying Liu ◽  
Haochuan Li ◽  
Kazuhiro Tanaka ◽  
Noriyuki Tsumaki ◽  
Yoshihiko Yamada
Keyword(s):  
Collagen Gene ◽  
Enhancer Sequence ◽  
First Intron

scholarly journals The transcriptional tissue specificity of the human proα1(I) collagen gene is determined by a negative cis-regulatory element in the promoter

1992 ◽  
Vol 286 (1) ◽  
pp. 179-185 ◽  
Author(s):  
C P Simkevich ◽  
J P Thompson ◽  
H Poppleton ◽  
R Raghow
Keyword(s):  
Tissue Specificity ◽  
Regulatory Element ◽  
Mesenchymal Cell ◽  
Cell Types ◽  
Regulatory Elements ◽  
Negative Influence ◽  
Collagen Gene ◽  
Specific Expression ◽  
Cis Acting ◽  
First Intron

The transcriptional activity of plasmid pCOL-KT, in which human pro alpha 1 (I) collagen gene upstream sequences up to -804 and most of the first intron (+474 to +1440) drive expression of the chloramphenicol acetyltransferase (CAT) gene [Thompson, Simkevich, Holness, Kang & Raghow (1991) J. Biol. Chem. 266, 2549-2556], was tested in a number of mesenchymal and non-mesenchymal cells. We observed that pCOL-KT was readily expressed in fibroblasts of human (IMR-90 and HFL-1), murine (NIH 3T3) and avian (SL-29) origin and in a human rhabdomyosarcoma cell line (A204), but failed to be expressed in human erythroleukaemia (K562) and rat pheochromocytoma (PC12) cells, indicating that the regulatory elements required for appropriate tissue-specific expression of the human pro alpha 1 (I) collagen gene were present in pCOL-KT. To delineate the nature of cis-acting sequences which determine the tissue specificity of pro alpha 1 (I) collagen gene expression, functional consequences of deletions in the promoter and first intron of pCOL-KT were tested in various cell types by transient expression assays. Cis elements in the promoter-proximal and intronic sequences displayed either a positive or a negative influence depending on the cell type. Thus deletion of fragments using EcoRV (nt -625 to -442 deleted), XbaI (-804 to -331) or SstII (+670 to +1440) resulted in 2-10-fold decreased expression in A204 and HFL-1 cells. The negative influences of deletions in the promoter-proximal sequences was apparently considerably relieved by deleting sequences in the first intron, and the constructs containing the EcoRV/SstII or XbaI/SstII double deletions were expressed to a much greater extent than either of the single deletion constructs. In contrast, the XbaI* deletion (nt -804 to -609), either alone or in combination with the intronic deletion, resulted in very high expression in all cells regardless of their collagen phenotype; the XbaI*/(-SstII) construct, which contained the intronic SstII fragment (+670 to +1440) in the reverse orientation, was not expressed in either mesenchymal or nonmesenchymal cells. Based on these results, we conclude that orientation-dependent interactions between negatively acting 5′-upstream sequences and the first intron determine the mesenchymal cell specificity of human pro alpha 1 (I) collagen gene transcription.

A 47-bp Sequence of the First Intron of the Mouse Proα1 (II) Collagen Gene Is Sufficient to Direct Chondrocyte Expression

1996 ◽  
Vol 785 (1) ◽  
pp. 284-287 ◽  
Author(s):  
VÉRonique Lefebvre ◽  
Krish Mukhopadhyay ◽  
Guang Zhou ◽  
Silvio Garofalo ◽  
Chad Smith ◽  
...  
Keyword(s):  
Collagen Gene ◽  
First Intron

Interferon-γ +874 Polymorphism in the First Intron of the Human Interferon-γ Gene and Kidney Allograft Outcome

2010 ◽  
Vol 42 (10) ◽  
pp. 4505-4508 ◽  
Author(s):  
J.C.O. Crispim ◽  
I.J. Wastowski ◽  
D.M. Rassi ◽  
C.T. Mendes-Junior Silva ◽  
C. Bassi ◽  
...  
Keyword(s):  
Interferon Γ ◽  
Human Interferon ◽  
Kidney Allograft ◽  
First Intron ◽  
Allograft Outcome

scholarly journals Interactions between the promoter and first intron are involved in transcriptional control of alpha 1(I) collagen gene expression.

1988 ◽  
Vol 8 (11) ◽  
pp. 4851-4857 ◽  
Author(s):  
P Bornstein ◽  
J McKay ◽  
D J Liska ◽  
S Apone ◽  
S Devarayalu
Keyword(s):  
Growth Hormone ◽  
Human Growth Hormone ◽  
Transcriptional Control ◽  
Rnase Protection Assay ◽  
Human Growth ◽  
Collagen Gene ◽  
Mrna Levels ◽  
3T3 Cells ◽  
Rnase Protection ◽  
First Intron

The first intron of the human collagen alpha 1(I) gene contains several positively and negatively acting elements. We have studied the transcription of collagen-human growth hormone fusion genes, containing deletions and rearrangements of collagen intronic sequences, by transient transfection of chick tendon fibroblasts and NIH 3T3 cells. In chick tendon fibroblasts, but not in 3T3 cells, inversion of intronic sequences containing a previously studied 274-base-pair segment, A274, resulted in markedly reduced human growth hormone mRNA levels as determined by an RNase protection assay. This inhibitory effect was largely alleviated when deletions were introduced in the collagen promoter of plasmids containing negatively oriented intronic sequences. Evidence for interaction of the promoter with the intronic segment, A274, was obtained by gel mobility shift assays. We suggest that promoter-intron interactions, mediated by DNA-binding proteins, regulate collagen gene transcription. Inversion of intronic segments containing critical interactive elements might then lead to an altered geometry and reduced activity of a transcriptional complex in those cells with sufficiently high levels of appropriate transcription factors. We further suggest that the deleted promoter segment plays a key role in directing DNA interactions involved in transcriptional control.

Regulation of liver carnitine palmitoyltransferase I gene expression by hormones and fatty acids

2001 ◽  
Vol 29 (2) ◽  
pp. 310-316 ◽  
Author(s):  
J.-F. Louet ◽  
C. Le May ◽  
J.-P. Pégorier ◽  
J.-F. Decaux ◽  
J. Girard
Keyword(s):  
Fatty Acids ◽  
Gene Transcription ◽  
Peroxisome Proliferator ◽  
Gene Encoding ◽  
First Intron ◽  
Transcriptional Effect ◽  
Carnitine Palmitoyltransferase I ◽  
Responsive Element ◽  
Cpt I ◽  
I Gene

This brief review focuses on the transcriptional regulation of liver carnitine palmitoyltransferase I (L-CPT I) by pancreatic and thyroid hormones and by long-chain fatty acids (LCFA). Both glucagon and 3,3′,5-tri-iodothyronine (T3) enhanced the transcription of the gene encoding L-CPT I, whereas insulin had the opposite effect. Interestingly, the transcriptional effect of T3 required, in addition to the thyroid-responsive element, the co-operation of a sequence located in the first intron of L-CPT I gene. Non-esterified fatty acids rather than acyl-CoA ester or intramitochondrial metabolite were responsible for the transcriptional effect on the gene encoding LCPT I. It was shown that LCFA and peroxisome proliferators stimulated L-CPT I gene transcription by distinct mechanisms. Peroxisome proliferator stimulated L-CPT I gene transcription through a peroxisome-proliferator-responsive element (PPRE) located at -2846 bp, whereas LCFA induced L-CPT I gene transcription through a peroxisome-proliferator-activated receptor α (PPARα)-independent mechanism owing to a sequence located in the first intron of the gene.

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