Functional Analysis of the 5′ Promoter Region of the Rat Lamin A Gene

Tiwari, Bhavna; Muralikrishna, Bh; Parnaik, Veena K.

doi:10.1089/dna.1998.17.957

Cited by 9 publications

(23 citation statements)

References 33 publications

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“…These findings suggested that the LMNA promoter might be active in all cells and that distinct regulatory elements serve to silence LMNA expression in undifferentiated cells. Later, Tiwari et al [51] showed that AP1 and SP1 sites in the 5′ promoter of rat Lmna are sufficient for the active transcription, and suggested that conformational changes in chromatin might underlie cell-type specific repression of Lmna expression.…”

Section: Regulation Of the A-type Laminsmentioning

confidence: 99%

Nuclear Lamins in the Brain — New Insights into Function and Regulation

et al. 2012

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The nuclear lamina is an intermediate filament meshwork composed largely of four nuclear lamins—lamins A and C (A-type lamins) and lamins B1 and B2 (B-type lamins). Located immediately adjacent to the inner nuclear membrane, the nuclear lamina provides a structural scaffolding for the cell nucleus. It also interacts with both nuclear membrane proteins and the chromatin and is thought to participate in many important functions within the cell nucleus. Defects in A-type lamins cause cardiomyopathy, muscular dystrophy, peripheral neuropathy, lipodystrophy, and progeroid disorders. In contrast, the only bona fide link between the B-type lamins and human disease is a rare demyelinating disease of the central nervous system—adult-onset autosomal-dominant leukoencephalopathy, caused by a duplication of the gene for lamin B1. However, this leukoencephalopathy is not the only association between the brain and B-type nuclear lamins. Studies of conventional and tissue-specific knockout mice have demonstrated that B-type lamins play essential roles in neuronal migration in the developing brain and in neuronal survival. The importance of A-type lamin expression in the brain is unclear, but it is intriguing that the adult brain preferentially expresses lamin C rather than lamin A, very likely due to microRNA-mediated removal of prelamin A transcripts. Here, we review recent studies on nuclear lamins, focusing on the function and regulation of the nuclear lamins in the central nervous system.

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Section: Regulation Of the A-type Laminsmentioning

confidence: 99%

Nuclear Lamins in the Brain — New Insights into Function and Regulation

et al. 2012

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“…These results suggest that cJun causes morphological transformation through direct or indirect transcriptional regulation of multiple genes related to the cytoskeleton and cell adhesion. The cytoskeletaland adhesion-related genes with the exception of collagen alpha 1 type 1 (Noti et al, 1996), annexin II (Braselmann et al, 1992), lamin A (Tiwari et al, 1998) and integrin alpha (also named p150 and CD11c) Lopez-Rodriguez et al, 1996;Noti et al, 1996), galectin 3 (Gaudin et al, 1997), and annexin I (Solito et al, 1998) represent novel targets of AP-1. These genes may cooperatively contribute to the observed morphological phenotypes by cJun.…”

Section: Identification Of Cjun-responsive Genesmentioning

confidence: 99%

Identification of cJun-responsive genes in Rat-1a cells using multiple techniques: increased expression of stathmin is necessary for cJun-mediated anchorage-independent growth

et al. 2003

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cJun is a major component of the transcription factor AP-1 and mediates a diverse set of biologic properties including proliferation, differentiation, and apoptosis. To identify cJun-responsive genes, we inducibly expressed cJun in Rat-1a cells and observed two distinct phenotypes: changes in cellular morphology with adherent growth and anchorage-independent growth. The biologic effects of cJun were entirely reversible demonstrating that they require the continued presence of cJun. To determine the genes, which mediate the biologic effects of cJun, we employed multiple methods including differential gene analysis, suppression subtractive hybridization, and cDNA microarrays. We identified 38 cJun-responsive genes including three uncharacterized genes under adherent and/or nonadherent conditions. Half of the known 36 genes were cytoskeleton-and adhesion-related genes, suggesting a major role of cJun in the regulation of the genes related to cell morphology. As proof of the principle that this approach could identify genes whose upregulation was necessary for nonadherent growth, we investigated one gene, stathmin whose upregulation by cJun was observed only under these conditions. Although overexpression of stathmin did not result in nonadherent growth, inhibition of stathmin protein expression by antisense oligonucleotides in cJun-induced Rat-1a cells prevented nonadherent growth. These results suggest that stathmin plays an essential role in anchorage-independent growth by cJun and may be a potential target for specific inhibitors for AP-1-dependent processes involved in carcinogenesis.

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“…Transfections of reporter plasmids and a b-galactosidase expression vector (pCH110 for NIH 3T3 and PCC-4 cells and pCMVSPORT bgal for CRL-1600 cells) were carried out as described [15,17]. Cells were lysed and aliquots were assayed for LUC activity using a kit from Promega Corporation (Madison, Wisconsin) and for b-galactosidase activity as described [21].…”

Section: Cell Culture and Dna Transfectionsmentioning

confidence: 99%

Cell‐type‐specific interactions at regulatory motifs in the first intron of the lamin A gene

2004

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Lamins A, C and C2 are alternatively spliced products of the LMNA gene; lamins A and C are expressed in differentiated somatic cells, whereas lamin C2 is expressed in germ cells. We have analyzed a segment of the first intron of the LMNA gene for cell-type-specific regulatory elements. We identified a 420-bp fragment that increased promoter activity in lamin A-expressing cells but repressed activity in undifferentiated cells. DNase I footprinting and electrophoretic mobility shift assays revealed two binding motifs, footprinted region A (FPRA) and FPRB. The hepatocyte nuclear factor-3b was bound to FPRA only in somatic cell extracts and this motif had an inhibitory effect on promoter activity. The retinoic X receptor b, RXRb, bound near FPRB with extracts from lamin A-or C2-expressing cells, and this site enhanced promoter activity. We have, thus, identified two novel binding sites for transcription factors in a region likely to function as an important regulatory element for the cell-type-specific transcription of A-type lamins.

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Functional Analysis of the 5′ Promoter Region of the Rat Lamin A Gene

Cited by 9 publications

References 33 publications

Nuclear Lamins in the Brain — New Insights into Function and Regulation

Nuclear Lamins in the Brain — New Insights into Function and Regulation

Identification of cJun-responsive genes in Rat-1a cells using multiple techniques: increased expression of stathmin is necessary for cJun-mediated anchorage-independent growth

Cell‐type‐specific interactions at regulatory motifs in the first intron of the lamin A gene

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