Structure of the gene encoding Peripherin, an NGF-regulated neuronal-specific type III intermediate filament protein

Thompson, Mary Ann; Ziff, Edward B.

doi:10.1016/0896-6273(89)90228-6

Cited by 146 publications

(105 citation statements)

References 67 publications

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“…The present study therefore reveals a functional attribute of neural gene promoters that is distinct from these models, since the core region of the I N promoter is capable of mafK transcriptional activation in neural tissues. Furthermore, the I N core region does not contain either NRSE or other elements that appear to be important for neural-specific gene regulation (Lewis & Cowan 1986;Thompson & Ziff 1989;Maue et al 1990;Lundel & Hirsh 1992;Mori et al 1992;Nevidi et al 1992;Clark & Mellon 1995;Liu & Fischer 1996;Uestuki et al 1996), suggesting that previously unidentified transcription factors may be responsible for mafK I N promoter activity.…”

Section: Discussionmentioning

confidence: 99%

A core region of the mafK gene I_N promoter directs neurone‐specific transcription in vivo

et al. 1998

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Background: MafK serves as a required subunit of erythroid transcription factor NF-E2 and also functions with various heterodimeric CNC family proteins. MafK expression begins in early mesoderm and is observed in mesenchymal and haematopoietic cells, as well as in neurones during mouse development. In mesodermal descendants, MafK mRNA begins with a distal first exon (called I M ), whereas the mRNA in neurones begins with a proximal first exon (I N ).

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Section: Discussionmentioning

confidence: 99%

A core region of the mafK gene I_N promoter directs neurone‐specific transcription in vivo

et al. 1998

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“…This response follows the transcriptional induction of the c-fos and Bactin genes at 30 min post-NGF treatment (Greenberg et al 1985(Greenberg et al , 1986. As expected, the late response gene, peripherin (Thompson and Ziff 1989), and other genes unresponsive to NGF during this time period (Greenberg et al 1985(Greenberg et al , 1986Leonard et al 1987) were not induced. The 10b gene, a second NGF-inducible delayed early gene of unknown function (Leonard et al 1987; E. Gizang-Ginsberg and E.B.…”

Section: Ngf Induction Of the Th Gene Is Transcriptionally Regulated mentioning

confidence: 99%

“…This class includes the tyrosine hydroxylase (TH) gene (Leonard et al 1987). A third class includes the peripherin gene, which encodes a neuron-specific intermediate filament protein (Portier et al 1984;Leonard et al 1987Leonard et al , 1988Parysek et al 1988;Thompson and Ziff 1989). Peripherin is representative of a class of "late" genes whose transcription is induced -18 hr post-NGF, a time coinciding with the onset of neurite extension.…”

mentioning

confidence: 99%

Nerve growth factor regulates tyrosine hydroxylase gene transcription through a nucleoprotein complex that contains c-Fos.

Gizang-Ginsberg¹,

Ziff²

1990

Genes Dev.

249

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We have studied nerve growth factor (NGF) regulation of the expression of the tyrosine hydroxylase (TH) gene in PC12 cells. The TH gene encodes the initial and rate-limiting enzyme of the catecholamine biosynthetic pathway. We show that the TH gene is transiently transcriptionally induced by a mechanism reliant on new protein synthesis during 1-2 hr of NGF stimulation, a time following the induction of the c-los gene at 15 min post-NGF treatment. A potential regulatory sequence located within the TH gene promoter, the TH-FSE, shares homology to a known regulatory element, the fat-specific element (FSE), which is found upstream from genes activated during adipocyte differentiation and binds the Fos-Jun transcription factor complex. We show that the TH-FSE DNA sequence elevates the basal level of transcription from the rat TH promoter and is required for NGF inducibility. This DNA element binds authentic Fos-Jun products produced by in vitro translation. We demonstrate further that the TH-FSE can bind proteins present in PC12 nuclear extracts in a sequence-specific manner. The DNA/nucleoprotein complex that forms increases in abundance during NGF stimulation and reaches a maximum level at 4 hr of treatment. Antibody inhibition studies utilizing an anti-Fos antibody indicate that Fos and/or Fos-related antigen(s) associate with the TH-FSE and suggest that the Fos protein family contributes to the regulation of TH in vivo. These results support a model in which NGF-induced immediate early genes, including c-Fos, contribute to the regulation of delayed early genes such as TH and thereby control neuronal differentiation.

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“…These regions were located at rat gene [(GenBank Accession no. M26232; Thompson and Ziff (1989) (Fig. 5, top).…”

Section: Which Regions Of Intron 1 Are Responsible For Cell Type-specmentioning

confidence: 99%

Intron 1 Is Required for Cell Type-Specific, But Not Injury-Responsive, Peripherin Gene Expression

et al. 2002

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The "primitive" neurons of the peripheral nervous system (PNS) have the remarkable ability to regenerate new fibers. This regenerative process requires a sequence of gene activation and repression that is poorly understood. One gene that is almost exclusively expressed in neurons of the PNS and is activated after nerve injury is the peripherin intermediate filament gene, but little is known about the genomic elements that control either its restricted expression or its response to nerve injury in adult mice. Previous studies suggested that both 5Ј flanking sequence and intragenic regions were required for cell typespecific and injury-specific expression. To determine which intragenic regions were critical, mice were generated that expressed peripherin transgenes lacking different introns. Analyses of these mice revealed that deletion of introns 2-8 had no effect on either the cell type-specific or injury-specific expression of the peripherin gene; however, the remaining intron, intron 1, differentially bound Sp1 transcription-related proteins/ protein complexes in extracts from peripherin-expressing and nonexpressing tissues. Furthermore, a transgene that lacked intron 1 was not expressed in many neurons that contain endogenous peripherin but was activated after injury. Thus, accurate cell type-specific peripherin gene expression in the PNS depends on elements within intron 1, but other sequences, most likely in the 5Јflanking region, are required for activating the peripherin gene in response to nerve injury.

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Structure of the gene encoding Peripherin, an NGF-regulated neuronal-specific type III intermediate filament protein

Cited by 146 publications

References 67 publications

A core region of the mafK gene I_N promoter directs neurone‐specific transcription in vivo

A core region of the mafK gene I_N promoter directs neurone‐specific transcription in vivo

Nerve growth factor regulates tyrosine hydroxylase gene transcription through a nucleoprotein complex that contains c-Fos.

Intron 1 Is Required for Cell Type-Specific, But Not Injury-Responsive, Peripherin Gene Expression

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Structure of the gene encoding Peripherin, an NGF-regulated neuronal-specific type III intermediate filament protein

Cited by 146 publications

References 67 publications

A core region of the mafK gene IN promoter directs neurone‐specific transcription in vivo

A core region of the mafK gene IN promoter directs neurone‐specific transcription in vivo

Nerve growth factor regulates tyrosine hydroxylase gene transcription through a nucleoprotein complex that contains c-Fos.

Intron 1 Is Required for Cell Type-Specific, But Not Injury-Responsive, Peripherin Gene Expression

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A core region of the mafK gene I_N promoter directs neurone‐specific transcription in vivo

A core region of the mafK gene I_N promoter directs neurone‐specific transcription in vivo