The nucleotide sequence of the chicken apo very low density lipoprotein II gene

Schip, Alfred D. van het; Meijlink, Frits; Strijker, R.; Gruber, M.; Vliet, A J van; Klundert, J. A. M. Van De; Ab, Geert

doi:10.1093/nar/11.9.2529

Cited by 44 publications

(16 citation statements)

References 40 publications

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“…Firstly, region N2, -11 agATGAGCAT -2, which shows a striking sequence similarity with a negative element of the frog vitellogenin B1 promoter, -138 ctATGAGCAT -129 (mismatches are in lower case), but is in a different position [24]. Secondly, region CS, -22 GCCAGTGTCT -12, which is exactly duplicated at a similar position in the chicken estrogendependent, oviduct-specific ovalbumin gene [25]. Furthermore, the minor TATA box T2 was mutated.…”

Section: Transfected Vldl-cat Reporter Plasmids Are Hormone-dependentmentioning

confidence: 99%

Cis‐acting elements reinforcing the activity of the estrogen‐response element in the very‐low‐density apolipoprotein II gene promoter

Schippers

Kloppenburg

Vanwaardenburg

et al. 1994

European Journal of Biochemistry

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The gene coding for chicken very low density apolipoprotein I1 (apoVLDLII) is expressed exclusively in liver in response to estrogen. Previous work in our laboratory identified several protein binding sites, identified by the letters A to F, and their cognate factors within the first 300 bp flanking the gene. Here we present an extensive functional analysis of the apoVLDLII promoter by gene transfer experiments using a chicken hepatoma cell line and cultured non-hepatic cells. Deletion analysis revealed that the -301 to -163-bp promoter region, comprising elements El, E2 and F, is sufficient for strong estrogen-dependent expression. Mutation analysis demonstrated that efficient transcription requires the interplay of the major estrogen response element E l with several other cis-acting elements. Analysis of individual protein binding sites showed that element El is sufficient by itself to confer weak estrogen-induced transcription from the apoVLDLII promoter, and that additional promoter elements are required for full estrogen-responsiveness. Elements F and B1 were capable of strongly potentiating the activity of element El. In general, the activity of certain cis-acting elements appeared to be strongly promoter-context dependent. Cultured non-liver cells expressed transfected VLDL-CAT reporter plasmids in the presence of cotransfected estrogen receptor expression vector in a hormone-dependent way, indicating that for the control of tissue specificity the 5'-proximal promoter region is not sufficient.

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Section: Transfected Vldl-cat Reporter Plasmids Are Hormone-dependentmentioning

confidence: 99%

Cis‐acting elements reinforcing the activity of the estrogen‐response element in the very‐low‐density apolipoprotein II gene promoter

Schippers

Kloppenburg

Vanwaardenburg

et al. 1994

European Journal of Biochemistry

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“…All other probes were derived from a 3.0-kb BgflI fragment which covers the larger part of the apo-VLDL II gene, and had been cloned in pBR322 [5]. The entire insert DNA was isolated [11,12] and nick-translated [13] to yield the socalled total probe.…”

Section: Preparation Of Dna Probesmentioning

confidence: 99%

“…Various probes, specific for the various introns, were obtained by cloning suitable fragments of the BgfiI clone. A 287-bp PstI fragment from intron A, and a 348-bp Sau3A fragment from intron C, were subcloned in M13mp9 bacteriophage DNA, as described earlier [5]. Single-stranded phage DNA was used as a template for Klenow polymerase to synthesize a probe which is complementary to RNA sequences in the intron A or intron C region.…”

Section: Preparation Of Dna Probesmentioning

confidence: 99%

“…Apo-VLDL II is a yolk protein made in large amounts in the liver of chickens upon estradiol stimulation. The gene, 2918 nt long [5], contains three introns [6]; the mRNA (excluding the poly(A) tail) is 656 nt long and codes for a protein of 106 amino acids [7]. The present paper shows that the excision of an intron does not require prior excision of This paper is dedicated to Prakash Datta as a token of gratitude and friendship * Present address: Molekularbiologie I, University of Zurich, Honggerberg, 8093 Zurich, Switzerland + To whom correspondence should be addressed…”

Section: Introductionmentioning

confidence: 99%

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Splicing pathways of the chicken apo very low density lipoprotein II (pre)messenger RNA

et al. 1986

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The precursor-mRNA transcribed from the chicken apo very low density lipoprotein II gene was identified. This gene which is under full estrogen control and only expressed in the liver, possesses three introns. Splicing intermediates were characterized by hybridization with intron-specific probes, and by electron microscopy of R-loops. The introns appear to be excised in a non-obligatory order, but at different rates. APO-VLDL ZZRNA splicing Estrogen Yolk protein gene

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“…36 These genes are at various stages of analysis in a number of laboratories. Nucleotide sequences for the avian apo II gene 37 and the human apo A-l gene 33 -M have been reported. Gene organization will be considered below.…”

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confidence: 99%

Molecular biology in arteriosclerosis research.

Williams¹

1985

Arteriosclerosis

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The topics discussed In this article illustrate how molecular biology will have a dramatic Impact on arteriosclerosis research. DNA clones for a small number of relevant proteins have been isolated, and studies are underway in numerous laboratories to extend these initial studies. The techniques of molecular biology will provide major advances in our understanding of numerous proteins directly or indirectly involved in the atherogenlc process. Cloning technology will solve the primary structures of many proteins that can not be purified In quantities sufficient for classical methods of analysis. Studies of regulation will benefit from the availability of DNA probes, the ability to generate site-directed antibodies, and the use of reverse genetics to Identify nucleic acid sequences involved in the regulation of gene expression. Studies of gene structure and genetic polymorphisms will unravel the genetic basis for defects In llpld and lipoprotein metabolism and should provide valuable reagents for clinical screening and diagnosis. The reverse genetics approach will permit the systematic analysis of structure-function relationships at the protein level In a manner not previously possible. Each of these will contribute to our understanding of the atherogenic process and should provide insight into ways of preventing and treating arteriosclerosis. T he purpose of this article is to explore how molecular biology can have an impact on research in the broad field of arteriosclerosis. The past few years have seen the techniques of molecular biology applied to an increasingly wider range of problems directly or indirectly related to arteriosclerosis. The first focus of research in this area has been the isolation and characterization of complementary DNA (cDNA) clones for the major apolipoproteins of the plasma lipoproteins. The apolipoproteins were prime targets for initial studies because they are abundant products of lipoprotein-producing tissues and the amino acid sequences of many of these proteins are known. While the current literature seems filled with cloning papers, we only have scratched the surface

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The nucleotide sequence of the chicken apo very low density lipoprotein II gene

Cited by 44 publications

References 40 publications

Cis‐acting elements reinforcing the activity of the estrogen‐response element in the very‐low‐density apolipoprotein II gene promoter

Cis‐acting elements reinforcing the activity of the estrogen‐response element in the very‐low‐density apolipoprotein II gene promoter

Splicing pathways of the chicken apo very low density lipoprotein II (pre)messenger RNA

Molecular biology in arteriosclerosis research.

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