Cloning and sequence analysis of a cDNA encoding rat preprocholecystokinin.

Deschenes, Robert J.; Lorenz, Lori J.; Haun, Randy S.; Roos, Bernard A.; Collier, Kenneth J.; Dixon, Jack E.

doi:10.1073/pnas.81.3.726

Cited by 286 publications

(112 citation statements)

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“…CCK (44-mer): 5 Ј -ATCCATCCAGCCCATGTAGTC-CCGGTCACTTATCCTGTGGCTAG-3 Ј according to nucleotides 351-395 of whole rat prepro-cholecystokinin cDNA (Deschenes et al 1984); BDNF (50-mer): 5 Ј -AGTTCCAGTGCCTTTTGTCTATGCCCCTGCAGC-CTTCCTTCGTGTAACCC-3 Ј according to nucleotides 645-694 of whole rat cDNA (Maisonpierre et al 1991); and NPY(48-mer) : 5 Ј -ATGAGATGTGGGGGGAAAC-TAGGAAAAGTCAGGAGAGCAAGTTTCATT-3 Ј according to nucleotides 3148-3195 of rat NPY sequence (Larhammar et al 1987).…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

Müller

Toschi

Kresse

et al. 2000

Neuropsychopharmacology

252

107

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Repetitive transcranial magnetic stimulation (rTMS) is increasingly used as a therapeutic tool in various neurological and psychiatric disorders, and we recently found that it has a neuroprotective effect both in vitro andTranscranial magnetic stimulation (TMS), a technique in which a time-varying strong electric current is applied through a coil held in direct contact with the subject's head, was originally developed for diagnostic use in neurology (for review see Rossini and Rossi 1998). A possible effect of TMS on mood was first reported in 1987 (Bickford et al. 1987) and, although discussed controversially, to date several lines of evidence resulting from both preclinical (Fleischmann et al. 1995;Zyss et al. 1997) and clinical (e.g., Pascual-Leone et al. 1996) studies support the notion that repetitive TMS (rTMS) may have antidepressant properties: rTMS induces transient enhancement of mood in healthy subjects, and daily application alleviates symptoms in patients suffering from treatment-resistant major depression (for review see George et al. 1999).Although rTMS is currently being evaluated as a possible alternative or add-on therapy in the treatment of refractory depression, knowledge concerning its effects at the molecular and cellular level is still very limited. Recently, Ji et al. (1998) reported a specific activation of brain regions in terms of immediate early gene expression in rats in response to rTMS. In addition, we provided a first evidence for a neuroprotective effect of long-term rTMS in vivo and in vitro (Post et al. 1999). The in vitro studies showed that magnetic stimulation analogous to TMS increased the overall viability of mouse monoclonal hippocampal HT22 cells and had a neuroprotective effect against oxidative stressors such as amyloid beta (A ␤ ) and glutamate. Moreover, the treatment increased the release of the potentially neuroprotective secreted amyloid precursor protein (sAPP) into the supernatant of HT22 cells and into cerebrospinal fluid from rats. Accordingly, HT22 cells preincubated with cerebrospinal fluid from long-term rTMStreated rats were found to be protected against A ␤ (Post et al. 1999). However, the neurochemical mechanisms underlying these neuroprotective properties as well as the putative therapeutic effects of rTMS in neurological and psychiatric disorders still remain to be elucidated.Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family and is abundantly expressed in the adult brain. The neurotrophic and also neuroprotective effects of BDNF have been characterized extensively both in vitro and in vivo. In addition, upregulation of BDNF has been implicated in neuronal responses to various kinds of injuries, such as epileptic seizures, cerebral ischemia, and hypoglycemia (for review see Connor and Dragunow 1998). Recent work raised the possibility that one of the many long-term effects of antidepressant treatment may be regulation of neurotrophins: antidepressant drug treatment and electroconvulsive seizures (ECS) were shown to marke...

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Section: In Situ Hybridizationmentioning

confidence: 99%

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

Müller

Toschi

Kresse

et al. 2000

Neuropsychopharmacology

252

107

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“…1). The only exception is the combined cleavage and amidation site just after CCK-8 [30] (fig.4). Certain differences in the proteolysis of the CCK precursor have been described in different tissues [70].…”

Section: Tissue-specific Expression Of Monobasic Specific Converting mentioning

confidence: 99%

The processing of peptide precursors

Schwartz

1986

FEBS Letters

229

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The classical conversion site in precursors of regulatory peptides is a sequence of two basic amino acids. During recent years, however, a group of monobasic cleavage sites has emerged. In certain cell systems it has been shown that the monobasic cleavage mechanism is both a specific mechanism which only attacks a particular basic residue, and a distinct mechanism which can be separated from the dibasic cleaving mechanism within the same cell. The vast majority of monobasic cleavages occur at single arginines although cleavage after a lysine residue has also been demonstrated. There is no ‘consensus sequence’ of amino acids surrounding the single basic residue which is the apparent signal for proteolytic processing. However, in approximately one third of the cases, a proline residue is found either just before or just after the basic residue. On the basis of this ‘proline‐directed arginyl cleavage’ it is discussed how the conformation of the peptide backbone might be important for this type of cleavage. Finally, it is suggested that tissue‐specific expression of different processing enzymes, e.g. dibasic and monobasic specific forms, might explain the tissue‐specific processing of precursors like the pro‐opiomelanocortin and the CKK. and somatostatin precursor.

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“…The first 100 bp 5Ј to the conventionally accepted transcription initiation site in rat (10,23), mouse (11), and man (16) have 80% homology. Sp1 consensus recognition sequence has been described in the human CCK promoter between Ϫ37 and Ϫ48 (16).…”

Section: Discussionmentioning

confidence: 99%

“…In the brain CCK is a neurotransmitter (8,9). There is a commonly accepted gut, as well as brain, CCK transcription initiation site in the rat (10), mouse (11), and man (12). Alternatively, more distal 5Ј CCK transcription start sites have been identified in the brain of the rat (13).…”

Section: Cholecystokinin (Cck)mentioning

confidence: 99%

“…These include phorbol ester (14 -16), cAMP (14,(17)(18)(19)(20), and gonadal steroids (21), as well as glucocorticoids (22). Several cis-elements, important in transcriptional control, have been identified within the first 119 bp of the 5Ј flanking region of the rat CCK gene (10). This 119-bp fragment contains a sequence homologous with a 12-Otetradecanoylphorbol 13-acetate (TPA)-responsive element of the c-fos gene, as well as a cAMP-responsive element identified in the proenkephalin gene (23).…”

Section: Cholecystokinin (Cck)mentioning

confidence: 99%

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Identification of Overlapping AP-2/NF-κB-responsive Elements on the Rat Cholecystokinin Gene Promoter

Katsel

Greenstein²

2001

Journal of Biological Chemistry

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In this study we evaluate both proximal and more distal transcriptional regulation of the 5 flanking region of the rat cholecystokinin gene in transfected GH3 (rat pituitary tumor) cells. Transcriptional activity was measured on the intact (؊400 to ؉73) 5 flanking region of cholecystokinin (CCK), as well as with DNA constructs, which were deleted in both the conventional 5 to 3, as well as an unconventional 3 to 5 direction. Our in vivo studies indicate complex phorbol ester and forskolin interactions in the 10-base pair region between ؊130 and ؊140. We conclude, there are at least two transcriptional factors involved in regulation of the rat CCK transcription in this region. In vitro studies utilizing heterologous nuclear (HeLa) extract, as well as purified transcription factors AP-2 and NF-B, identify overlapped AP-2-and NF-B-responsive elements within the 17-base pair sequence between ؊149 and ؊134 of the distal 5 flanking region. In this region complex transcriptional regulation occurs, which indicates inhibition of AP-2 CCK promoter complexing by NF-B. Sixpoint mutations introduced into this sequence prevent AP-2 and NF-B binding to CCK promoter, as well as its transcriptional activation by phorbol ester and forskolin in GH3 cells. Cholecystokinin (CCK),1 a prototypical brain-gut peptide (1-5), has hemacrine (3, 6) and autocrine (7) action in the gut. In the brain CCK is a neurotransmitter (8, 9). There is a commonly accepted gut, as well as brain, CCK transcription initiation site in the rat (10), mouse (11), and man (12). Alternatively, more distal 5Ј CCK transcription start sites have been identified in the brain of the rat (13). Transcriptional control of CCK is regulated by multiple factors. These include phorbol ester (14 -16), cAMP (14,(17)(18)(19)(20), and gonadal steroids (21), as well as glucocorticoids (22). Several cis-elements, important in transcriptional control, have been identified within the first 119 bp of the 5Ј flanking region of the rat CCK gene (10). This 119-bp fragment contains a sequence homologous with a 12-Otetradecanoylphorbol 13-acetate (TPA)-responsive element of the c-fos gene, as well as a cAMP-responsive element identified in the proenkephalin gene (23). This sequence binds several transcription factors including AP-1, jun, and fos homodimers, as well as cAMP-responsive element-binding protein (16,19). Two other recognition sites on the human CCK gene are Sp1 (at Ϫ39 to Ϫ34) and E-box or upstream stimulatory factor (at Ϫ97 to Ϫ92) (16). Additionally, a negative interaction was detected between TPA-responsive element and E-box or upstream stimulatory factor-responsive element (24).TPA and forskolin activate specific nuclear proteins, which regulate gene transcription. These proteins include AP-2 (25) and NF-B (26, 27). Transcription factor AP-2 is activated either directly or indirectly by two signal transduction pathways (25). One route involves cAMP-dependent protein kinase A. The other involves phorbol ester and diacylglycerol-activated protein kinase C (28). AP-2 specifi...

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Cloning and sequence analysis of a cDNA encoding rat preprocholecystokinin.

Cited by 286 publications

References 40 publications

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

Long-Term Repetitive Transcranial Magnetic Stimulation Increases the Expression of Brain-Derived Neurotrophic Factor and Cholecystokinin mRNA, but not Neuropeptide Tyrosine mRNA in Specific Areas of Rat Brain

The processing of peptide precursors

Identification of Overlapping AP-2/NF-κB-responsive Elements on the Rat Cholecystokinin Gene Promoter

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