N-myc Regulates Parkin Expression

West, Andrew B.; Kapatos, Gregory; O’Farrell, Casey; Gonzalez-de-Chavez, Fanny; Chiu, Kelvin; Farrer, Matthew J.; Maidment, Nigel T.

doi:10.1074/jbc.m400126200

Cited by 51 publications

(27 citation statements)

References 34 publications

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“…This finding is consistent with a number of reported studies. Blackwell et al (52) and Cohn and co-workers (48) found that N-MYC protein could bind with numerous variant E-box sites including CATGCG, and other investigators have demonstrated that N-MYC binds and activates various promoters in the face of other E-box sequences (39,46). Our current study used three different methods including luciferase promoter-reporter assays, ChIP, and EMSA assays to demonstrate N-MYC binding to the FAK promoter.…”

Section: Discussionmentioning

confidence: 99%

N-MYC Regulates Focal Adhesion Kinase Expression in Human Neuroblastoma

Beierle

Trujillo

Nagaram

et al. 2007

Journal of Biological Chemistry

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N-MYC is a transcription factor important for the control of cellular differentiation and proliferation (1, 2). It is normally expressed in the brain and peripheral nervous system (1). N-MYC has been shown to influence the differentiation of neural crest cells. Early in mouse embryogenesis, N-MYC is present primarily in the migrating neural crest cells, but as the embryo matures, the expression of N-MYC becomes limited to those cells that are undergoing neuronal differentiation (3). Abnormal expression of N-MYC is most notably associated with the pediatric tumor of neural crest origin, neuroblastoma. Amplification of the N-MYC oncogene is the primary adverse prognostic indicator in human neuroblastoma (4, 5). The level of N-MYC expression has been shown to correlate with the growth (6 -9) and invasiveness (10) of neuroblastoma cells, and transgenic mice with N-MYC overexpression develop spontaneous neuroblastoma tumors (11). In addition, down-regulation of N-MYC with antisense oligonucleotides leads to decreases in both cellular proliferation and in anchorageindependent growth in the neuroblastoma cells (6, 9). Despite this information, the exact function and transcriptional gene targets of N-MYC in neuroblastoma are currently not well characterized (5).Focal adhesion kinase (FAK) 3 is a nonreceptor cytoplasmic 125-kDa protein-tyrosine kinase. Initial studies revealed that both the transcription of FAK mRNA (12) and the expression of FAK protein (13-19) are significantly increased in primary and metastatic breast, colon, and thyroid tumors compared with normal tissues and that these changes occur early in tumorigenesis. Real time PCR analysis of colorectal carcinoma and liver metastasis with matched normal colonic tissues demonstrated increased FAK mRNA abundance in the tumors and metastatic tissues compared with control tissues (20), suggesting that the increased FAK expression in human tumors occurs at the level of transcription. Recently the FAK promoter was cloned and characterized, and transcriptional regulation of the FAK promoter has been demonstrated (21).FAK controls a number of cell signaling pathways including proliferation, viability, motility, and survival (22-25). The inhibition of FAK with antisense oligonucleotides has been shown to cause decreased growth in tumor cells (26). In addition, FAK inhibition with a dominant-negative FAK protein (FAK-CD) inhibited cell growth in human melanoma cells (12) and in * The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

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Section: Discussionmentioning

confidence: 99%

N-MYC Regulates Focal Adhesion Kinase Expression in Human Neuroblastoma

Beierle

Trujillo

Nagaram

et al. 2007

Journal of Biological Chemistry

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“…Primers from within the APP promoter, APP5e (exon 5) and APP18i (the intron after exon 18) were used in Sleegers et al 9 Primers for the control genes hemoglobin beta (HBB) on chromosome 11, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) on chromosome 12 and ubiquitin C (UBC) on chromosome 12, have previously been used in Johnson et al, 14 West et al 15 and in Sleegers et al, 9 respectively.…”

Section: Allele Quantificationmentioning

confidence: 99%

Low prevalence of APP duplications in Swedish and Finnish patients with early-onset Alzheimer's disease

et al. 2007

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Familial early-onset Alzheimer's disease with cerebral amyloid angiopathy (EOAD/CAA) was recently associated with duplications of the gene for the amyloid-b precursor protein (APP). In this study, we have screened for duplications of APP in patients with EOAD from Sweden and Finland. Seventy-five individuals from families with EOAD and 66 individuals with EOAD without known familial inheritance were screened by quantitative PCR. On the basis of the initial results, a portion of the samples was also investigated with quantitative multiplex PCR. No duplications of APP were identified, whereby we conclude that this is not a common cause of EOAD in the Swedish and Finnish populations, at least not in our collection of families and cases.

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“…cDNA was generated from the extracted RNA samples using a commercially available reverse transcription system (Promega) and evaluated by real-time PCR using Platinum SYBR Green Kit (Invitrogen) in a Bio-Rad IQ5 RealTime PCR Detection System following the manufacturers' protocols. The following primers were used: neomycin selection cassette of the Alu construct: 59-CCTCGGCCTCTGAGCTATTC-39 and 59-AGTCCCTTCCCGCTTCAGTGACAAC-39, and GAPDH: 59-GAAAT CCCATCACCATCTTCCAGG-39 and 59-GAGCCCCAGCCTTCTC CATG-39 (West et al 2004). Quantitation of the RNA from each heterogeneity construct was performed relative to the A30 control.…”

Section: Real-time Reverse Transcriptase Pcrmentioning

confidence: 99%

Diverse cis factors controlling Alu retrotransposition: What causes Alu elements to die?

Comeaux¹,

Roy-Engel²,

Hedges³

et al. 2009

Genome Res.

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The human genome contains nearly 1.1 million Alu elements comprising roughly 11% of its total DNA content. Alu elements use a copy and paste retrotransposition mechanism that can result in de novo disease insertion alleles. There are nearly 900,000 old Alu elements from subfamilies S and J that appear to be almost completely inactive, and about 200,000 from subfamily Y or younger, which include a few thousand copies of the Ya5 subfamily which makes up the majority of current activity. Given the much higher copy number of the older Alu subfamilies, it is not known why all of the active Alu elements belong to the younger subfamilies. We present a systematic analysis evaluating the observed sequence variation in the different sections of an Alu element on retrotransposition. The length of the longest number of uninterrupted adenines in the A-tail, the degree of A-tail heterogeneity, the length of the 3′ unique end after the A-tail and before the RNA polymerase III terminator, and random mutations found in the right monomer all modulate the retrotransposition efficiency. These changes occur over different evolutionary time frames. The combined impact of sequence changes in all of these regions explains why young Alus are currently causing disease through retrotransposition, and the old Alus have lost their ability to retrotranspose. We present a predictive model to evaluate the retrotransposition capability of individual Alu elements and successfully applied it to identify the first putative source element for a disease-causing Alu insertion in a patient with cystic fibrosis.

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N-myc Regulates Parkin Expression

Cited by 51 publications

References 34 publications

N-MYC Regulates Focal Adhesion Kinase Expression in Human Neuroblastoma

N-MYC Regulates Focal Adhesion Kinase Expression in Human Neuroblastoma

Low prevalence of APP duplications in Swedish and Finnish patients with early-onset Alzheimer's disease

Diverse cis factors controlling Alu retrotransposition: What causes Alu elements to die?

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