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PubMed2006

Increased frequency of aberrations in the p53/MDM2/p14(ARF) pathway in neuroblastoma cell lines established at relapse.

p53 mutations have been reported in cell lines derived from relapsed neuroblastoma tumors. We hypothesize that functional inactivation of p53 by mutation or other mechanisms is common in relapsed neuroblastoma and can contribute to chemoresistance. Our aim was to determine the frequency of p53 mutations, p14(ARF) methylation, or deletion and MDM2 amplification in 23 neuroblastoma cell lines (6 derived at diagnosis and 17 derived at relapse). One cell line was p53 mutant (BE2c) and two cell lines were deleted for p14(ARF) (LAN-6 and SHEP). Two cell lines were methylated for p14(ARF) (GIMEN and PER-108), one of which had low levels of p14(ARF) mRNA expression which increased following demethylation with 5-aza-2/deoxycytidine treatment (GIMEN), and four cell lines were confirmed to be MDM2-amplified. All these cell lines were derived from neuroblastomas at relapse. Inactivation of the p53 pathway was observed in 9 out of 17 neuroblastoma cell lines (53%) established at relapse and in none of the cell lines established from pretreatment tumors. If these data are confirmed in neuroblastoma tumors, this suggests that p53-independent therapy and reactivation of inactive p53 approaches would be useful in the management of relapsed neuroblastoma.

Cell Line, Tumor↗
PubMed2003

Contribution of germline mutations in BRCA2, P16(INK4A), P14(ARF) and P15 to uveal melanoma.

PURPOSE: Reports suggest that a subset of uveal melanoma is familial. The association of uveal melanoma with breast and ovarian cancer and the increased risk in BRCA2-linked families implicates germline BRCA2 mutations as the cause of a subset of uveal melanomas. Similarly, the association between cutaneous and uveal melanomas in some families, coupled with the high frequency of somatic deletions of the INK4A-ARF locus in uveal melanomas, strongly suggests that mutations in P16(INK4A) and P15 account for a proportion of uveal melanomas. METHODS: To examine this proposition, a systematically ascertained series of 385 patients with uveal melanoma were screened for germline mutations in BRCA2, P16(INK4A), P14(ARF), and P15. RESULTS: One patient was found to harbor a Gly35Ala substitution in exon 1alpha of P16(INK4A), which has previously been reported to be pathogenic. No mutations were detected in P14(ARF) or P15. None of the patients harbored germline nucleotide changes that lead to truncation or that create or disrupt consensus splice sites of BRCA2 or missense variants with clear pathogenic potential. CONCLUSIONS: These findings suggest that less than 2% of cases of uveal melanoma can be ascribed to germline mutations in BRCA2, P16(INK4A), P14(ARF), or P15. It is likely that mutations in other genes contribute to an inherited predisposition to uveal melanoma.

Adult↗
PubMed2002

A developmentally regulated ARF-like 5 protein (ARL5), localized to nuclei and nucleoli, interacts with heterochromatin protein 1.

ARF-like proteins (ARLs) are distinct group of members of the ARF family of Ras-related GTPases. Although ARLs are very similar in primary structure to ARFs, their functions remain unclear. We cloned mouse (m) and human (h) ARL5 cDNAs to characterize the protein products and their molecular properties. mARL5 mRNA was more abundant in liver than in other adult tissues tested. mARL5, similar to mARL4, was developmentally regulated and localized to nuclei. hARL5 interacted with importin-alpha through its C-terminal bipartite nuclear localization signal. When expressed in COS-7 cells, mutant hARL5(T35N), which is predicted to be GDP bound, was concentrated in nucleoli. The N-terminus of hARL5, like that of ARF, was myristoylated. Yeast two-hybrid screening and in vitro protein-interaction assays showed that hARL5(Q80L), predicted to be GTP bound, interacted with heterochromatin protein 1alpha (HP1alpha), which is known to be associated with telomeres as well as with heterochromatin, and acted as a transcriptional suppressor in mammalian cells. The interaction was reproduced in COS cells, where hARL5(Q80L) was co-immunoprecipitated with HP1alpha. hARL5 interaction with HP1alpha was dependent on the nucleotide bound, and required the MIR-like motif. Moreover, hARL5(Q80L), but not hARL5 lacking the MIR-like motif, was partly co-localized with overexpressed HP1alpha. Our findings suggest that developmentally regulated ARL5, with its distinctive nuclear/nucleolar localization and interaction with HP1alpha, may play a role(s) in nuclear dynamics and/or signaling cascades during embryonic development.

ADP-Ribosylation Factors↗
PubMed2005

The Arf GAPs AGAP1 and AGAP2 distinguish between the adaptor protein complexes AP-1 and AP-3.

ADP ribosylation factors (Arf) regulate membrane trafficking at multiple intracellular sites by recruiting coat proteins to membranes. The site-specific regulation of Arf is thought to be mediated by regulatory proteins including the guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Here, we test this hypothesis by comparing the site of action of the Arf GAP AGAP2 to the closely related AGAP1. AGAP1 has previously been found to associate with the adaptor protein complex AP-3 and regulate the function of AP-3 endosomes. We found that AGAP2 directly interacted with AP-1. AGAP2 colocalized with AP-1, transferrin receptor and Rab4 on endosomes. Overexpression of AGAP2 changed the intracellular distribution of AP-1 and promoted Rab4-dependent fast recycling of transferrin. Based on these results, we concluded that the closely related Arf GAPs, AGAP1 and AGAP2, distinguish between these related heterotetrameric adaptor protein complexes to specifically regulate AP-3 endosomes and AP-1 recycling endosomes.

ADP-Ribosylation Factors↗
PubMed2000

ARF- and coatomer-mediated peroxisomal vesiculation.

The authors characterized on a molecular level the clofibrate-inducible 26-kDa integral peroxisomal membrane protein (Pmp26p, Pex11-1p) of rat liver. By screening cDNA databases with the obtained Pex11-1p-cDNA, a second homologous cDNA was identified that codes for a polypeptide with slightly larger molecular mass than Pex11-1p. The authors call this polypeptide Pex11-2p. Studies on the topology of Pex11-1p revealed two transmembrane domains with the N- and C-terminus facing the cytoplasm. The C-terminal tail of Pex11-1p ends in a consensus dilysine motif of the type -KXKXX-COOH, which is known to be involved in the ADP-ribosylation factor (ARF)1-coat protein (COP) I coat (ARF)1-dependent membrane recruitment to Golgi membranes. Studies with isolated peroxisomes incubated in the presence of cytosol, adenosine triphosphate and GTP gamma S, indeed, provided evidence for specific binding of ARF and coatomer to peroxisomes. Expression of Pex11-1p in Chinese hamster ovary (CHO) wild-type cells led to a twofold increase in the number of peroxisomes, but expression in a temperature-sensitive CHO mutant, defective in coatomer, induced elongation and tubulation of peroxisomal structures, rather than numerical proliferation. The obtained results for the first time offer a mechanism explaining Pex11-1p-, as well as ARF- and coatomer-mediated peroxisomal vesiculation. Two models are presented that may explain how these observations fit in with peroxisome biogenesis.

ADP-Ribosylation Factor 1↗
PubMed2006

Specific contribution of p19(ARF) to nitric oxide-dependent apoptosis.

NO is an important bioactive molecule involved in a variety of physio- and pathological processes, including apoptosis induction. The proapoptotic activity of NO involves the rise in the tumor suppressor p53 and the accumulation and targeting of proapoptotic members of the Bcl-2 family, in particular Bax and the release of cytochrome c from the mitochondria. However, the exact mechanism by which NO induces p53 activation has not been fully elucidated. In this study, we describe that NO induces p19(ARF) through a transcriptional mechanism. This up-regulation of p19(ARF) activates p53, leading to apoptosis. The importance of p19(ARF) on NO-dependent apoptosis was revealed by the finding that various cell types from alternate reading frame-knockout mice exhibit a diminished response to NO-mediated apoptosis when compared with normal mice. Moreover, the biological relevance of alternative reading frame to p53 apoptosis was confirmed in in vivo models of apoptosis. Together, these results demonstrate that NO-dependent apoptosis requires, in part, the activation of p19(ARF).

Animals↗
PubMed2000

Induction of apoptosis in human esophageal cancer cells by sequential transfer of the wild-type p53 and E2F-1 genes: involvement of p53 accumulation via ARF-mediated MDM2 down-regulation.

Transcriptional factor E2F-1 as well as tumor suppressor p53 have been shown to cause apoptosis independently in some types of human cancer cells when overexpressed. Here we report that sequential transfer of the wild-type p53 and E2F-1 genes efficiently induces apoptosis in human esophageal cancer cells and that E2F-1 overexpression directly, activates expression of p14 (ARF), which inhibits MDM2-mediated p53 degradation, resulting in the stabilization of p53. Infection of human esophageal cancer cell lines T.Tn and TE8 with adenovirus vector-expressing E2F-1 (Ad-E2F-1) enhanced mRNA and protein expression of ARF and decreased MDM2 protein expression. Transfection of ARF plasmid decreased MDM2 protein expression, which in turn increased p53 protein expression. Infection of T.Tn and TE8 cells first with adenovirus-expressing wild-type p53 (Ad-p53) and then with Ad-E2F-1 resulted in rapid induction of apoptosis; in contrast, simultaneous infection with Ad-E2F-1 and Ad-p53 had no significant antitumor effect. As shown by Western blot analysis, infection with suboptimal concentrations of Ad-E2F-1 induced the accumulation of exogenous p53 transduced by suboptimal concentrations of Ad-p53. Moreover, Ad-E2F-1-mediated ARF expression inhibited the up-regulation of MDM2 by overexpressed p53 in TE8 cells. Thus, overexpression of ectopic E2F-1 protein may stabilize endogenous as well as ectopic p53 protein via the E2F-1/ARF/MDM2/p53 regulatory pathway and, in this way, render cells more sensitive to apoptosis, an outcome that has important implications for the treatment of human esophageal cancers.

Adenoviridae↗
PubMed2003

Detecting homozygous deletions in the CDKN2A(p16(INK4a))/ARF(p14(ARF)) gene in urinary bladder cancer using real-time quantitative PCR.

PURPOSE: 9p21 is a major target in the pathogenesis of human urinary bladder cancer. The locus harbors the CDKN2A/ARF tumor suppressor gene, which encodes two cell cycle regulatory proteins cyclin dependent kinase 2A (p16(INK4a)) and alternate reading frame (p14(ARF)). We have designed a real-time quantitative PCR (QPCR) application to study homozygous deletion (HD) of CDKN2A/ARF in 186 urinary bladder cancer patients. EXPERIMENTAL DESIGN: Real-time QPCR, based on simultaneous amplification of ARF and a reference gene, GAPDH, was developed and evaluated in three melanoma cell lines with HDs at the CDKN2A/ARF locus (IGR-1, SK-MEL-5, and WM-266-4). In addition, loss of heterozygosity was analyzed at the D9S942, D9S1748, and D12S99 markers. Mutation analysis of the CDKN2A/ARF gene was performed using single-strand conformational polymorphism and sequencing. Results from the present investigation were combined with previous p53 analysis of the same urinary bladder neoplasms. RESULTS: Real-time QPCR analysis showed 26 (14%) HDs, 22 (12%) hemizygous deletions, and 3 (2%) multiple duplications. Loss of heterozygosity was determined in 30 (22%) cases at the D9S942 locus, which is located between E1alpha and E1beta of the CDKN2A/ARF gene. No association was established between occurrence of genetic aberrations at 9p21 and tumor stage or grade, supporting previous suggestions that CDKN2A/ARF inactivation is an early event in bladder carcinogenesis. CONCLUSIONS: We have established a fast and efficient method for detection of HDs. Our data support the notion that inactivation, including HDs, of CDKN2A/ARF is an early event in transitional cell carcinoma. We observed separate and specific targeting of the CDKN2A and ARF genes, respectively, and that simultaneous inactivation of ARF and p53 occurs.

Carcinoma, Transitional Cell↗
PubMed1992

[Mechanisms and therapeutic effect of Cordyceps sinensis (CS) on aminoglycoside induced acute renal failure (ARF) in rats].

Nephrotoxic ARF model of rat was induced by IP injection of either Gentamycin or Kanamycin and treated with CS. The results of study showed that the simultaneous administration of CS with Gentamycin could protect the proximal tubular cells from Gentamycin toxicity and the use of CS after the establishment of Kanamycin nephrotoxic ARF could prompt an earlier recovery from ARF as compared with the control group. The possible mechanisms of CS on ARF include: (1) protecting tubular cell sodium pump activity; (2) attenuating tubular cell lysosome overfunction stimulated by phagocytosis of aminoglycoside; (3) decreasing tubular cell lipoperoxidation in response to toxic injury.

Acute Kidney Injury↗
PubMedDate not supplied

[Clinical management of the patient affected with acute renal failure (ARF) secondary to volume depletion].

Most cases of ARF are secondary to volume depletion. In the literature, very few scientific publications address the problem of what to do when confronted with such a patient. As regarding the diagnosis of hypovolemia, an accurate history and physical examination can help to determine both the presence and etiology of volume depletion; postural hypotension (decrement in systolic blood pressure of more than 20 mmHg after standing from the supine position), associated with a pulse increment of 30 beats/min or more and dizziness are specific symptoms of hypovolemia. Laboratory indices are useful to diagnose volume depletion, but their interpretation is not simple, and they may not be available in the non-nephrologic environment. Fluid replacement therapy in hypovolemia is largely dependent upon the type of fluid that has been lost and concurrent electrolytic and acid-base disorders. Patients with hypernatremia and volume depletion should receive mild hypotonic solutions, whereas those with hyponatremia and hypovolemia should receive mild hypertonic solutions. The entity of reinfusion depends on daily losses. Conversely, monitoring of body weight can be considered an adequate index of fluid balance. Concerning the treatment of ARF, the use of loop diuretics in the early phases of pre-renal ARF decrease oxygen consumption in the tubular cells by inhibiting transcellular sodium transport, therefore preventing or limiting ischemic cell injury. The use of loop diuretics should also be evaluated in intermediate syndrome and ischemic NTA where diuretics can, respectively, reduce renal ischemia and convert oliguric ARF into the non-oliguric form.

Acute Kidney Injury↗
PubMed1993

The small GTP-binding proteins Rab4 and ARF are associated with released exosomes during reticulocyte maturation.

During maturation of reticulocytes to erythrocytes, small vesicles, termed exosomes, are released into the extracellular medium. GTP-binding proteins associated with exosomes were identified by separating proteins by sodium dodecyl sulfate polyacrylamide gel electrophoresis, transferring the proteins to nitrocellulose, and probing the blots with [alpha-32P]GTP. At least three GTP-binding proteins were detected with a molecular mass of 27, 26, and 20 kDa. Binding of GTP by exosomes was resistant to trypsin in the absence, but not in the presence of detergent. This indicates that the GTP-binding proteins are within the lumen of exosomes. During reticulocyte maturation, the amount of GTP-binding proteins released from reticulocytes was proportional to the amount of exosomes released. Western blot analysis demonstrated that the 27 kDa, 26 kDa, and 20 kDa proteins were Rab5p, Rab4p and ADP-ribosylation factor (ARF), respectively. In reticulocytes, Rab4p was highly enriched in exosomes and endosomes compared to plasma membrane and cytosol. Although mainly cytosolic, ARF was also found associated with endosomes and exosomes but not with plasma membrane. In contrast to Rab4p and ARF, Rab5p was enriched in the plasma membrane compared to cytosol, exosomes and endosomes. As exosomes are believed to derive from endosomes, Rab4p and ARF may be involved in the mechanism of exosome formation.

ADP-Ribosylation Factors↗
PubMed1997

ArF excimer laser irradiation of human dentin.

BACKGROUND AND OBJECTIVE: The use of excimer lasers for treatment of dental hard tissues has considerable potential because the combined characteristics of low wavelength and short pulse result in limited heat diffusion and, therefore, tissue ablation without the problems of collateral damage. To date, there are relatively few published studies concerning the effects of excimer laser irradiation on dental hard tissues. Thus the present study was conducted to examine the morphological changes in tooth dentin subsequent to ArF excimer laser irradiation. STUDY DESIGN/MATERIALS AND METHODS: The morphologic changes induced in normal, nondiseased human dentin following irradiation by an ArF excimer laser at fluences ranging from 1 to 4 J/cm2 and the number of laser pulses ranging from 50 to 1,000 were evaluated by scanning electron microscopy. RESULTS: Two modes of ablation, photochemical at low fluences and thermal at high fluences, were observed. A fluence of 1 J/ cm2 when combined with 50 or 100 pulses produced a uniform ablation of the dentin surface without signs of tissue melting. At fluences > 1.5 J/cm2, the thermal mode of ablation was more efficient at removing intertubular dentin than peritubular dentin. Further, when compared to the lower fluences, the higher settings produced a rougher ablation crater surface. Additionally, the higher fluences produced surface melting with each pulse and sealing of exposed dentinal tubules after irradiation with 100-300 laser pulses. CONCLUSIONS: The photochemical and thermal mechanisms of tooth dentin ablation were identified based on significant differences in tissue morphology following laser irradiation. The rates of tissue ablation and the observed morphologic changes indicate that the ArF excimer laser could be useful for caries removal and sealing of exposed dentinal tubules.

Dentin↗
PubMed2006

Differential effect of epigenetic alterations and genomic deletions of CDK inhibitors [p16(INK4a), p15(INK4b), p14(ARF)] in mantle cell lymphoma.

Mantle cell lymphoma (MCL) is characterized by the chromosomal translocation t(11;14)(q13;q32), resulting in overexpression of CCND1 in the vast majority of cases. In addition, alterations of other cell-cycle-regulating signal pathways (CDKN2B/CDKN2A-CCND1 and ARF-MDM2-TP53) are frequently observed. However, the hierarchy of promoter methylations and genomic alterations as well as the interaction with other cell-cycle regulator CDKN1A is poorly understood. A complete methylation-specific PCR coupled with direct sequencing of 71 MCL patient samples previously characterized for TP53 alterations, Ki67 expression by immunohistochemistry, and other genomic alterations was performed. In contrast to rare p16(INK4a) promoter methylation (9%), frequent p15(INK4b) (62%) and p14(ARF) (70%) promoter methylation was detectable in MCL. In an additional 16% of MCL cases, LOH for p16(INK4a) was detected. However, MCL cases with p15(INK4b) methylation tended to have lower proliferation (73% vs. 57%), and p15(INK4b) and p14(ARF) promoter methylation was also detected in normal stem cells. Therefore, epigenetic changes of those genes seem not to represent primary oncogenic mechanisms but physiological mechanisms of cell regulation. The rare p16(INK4a) promoter methylation and p16(INK4a) genetic alterations were directly correlated to cell proliferation and therefore are regarded as additional molecular alterations involved in the cell-cycle dysregulation of MCL.

Base Sequence↗
PubMed2001

Changes in p14(ARF) do not play a primary role in human chondrosarcoma tissues.

The locus encoding the tumor suppressor p16 has been found to code for a second, different protein. This protein, p14(ARF), has been shown to protect p53 from degradation. Like p16, its gene is often altered in different cancers. In this study, the first unique exon, exon 1 beta, of p14(ARF), has been studied in 22 chondrosarcoma tissues using polymerase chain reaction, DNA sequencing and methylation-specific polymerase chain reaction. One chondrosarcoma was found to have exon 1 beta homozygously deleted, but neither mutations nor methylations were found in any of the chondrosarcomas. This indicates that genetic changes of p14(ARF) are a rare event in chondrosarcoma.

Base Sequence↗
PubMed2005

Physico-chemical changes of human enamel irradiated with ArF excimer laser.

BACKGROUND AND OBJECTIVES: Irradiation of tooth enamel by lasers can alter its structure and chemical composition. The purpose of this work was to determine the compositional changes and to elucidate the mechanisms of laser-enamel interaction using ArF excimer laser. STUDY DESIGN/MATERIALS AND METHODS: Human enamel irradiated with ArF excimer laser (wavelength, 193 nm) at different fluences, was examined using X-ray diffraction, infrared (IR) spectroscopy and microprobe analysis. RESULTS: Ablation without significant compositional changes in irradiated enamel was evident when low fluences (approximately 200-380 mJ/cm2) were used. However, fluences between 640 and 2,300 mJ/cm2 resulted in an increased Ca/P ratio, decreased amount of carbonate and protein, and the formation of tricalcium phosphate and tetracalcium phosphate, suggesting the involvement of a photothermal mechanism. CONCLUSIONS: The results show that ArF excimer laser can alter the chemical composition and morphology of the highly mineralized (96%) dental enamel, depending on the fluence used.

Calcium↗
PubMed2001

Characterization of the CDKN2A and ARF genes in UV-induced melanocytic hyperplasias and melanomas of an opossum (Monodelphis domestica).

We examined the involvement of the cyclin-dependent kinase inhibitor 2A (CDKN2A) locus in the pathogenesis of ultraviolet (UV) radiation-induced melanomas in an opossum (Monodelphis domestica) melanoma model in which suckling young were exposed to UVB to produce melanocytic lesions. Monodelphis CDKN2A and alternated reading frame (ARF) cDNAs were cloned and sequenced, and the expression patterns of these genes were determined by reverse transcription-polymerase chain reaction in normal tissues, 39 primary melanocytic skin lesions, and two tumor-derived cell lines, one nonmetastatic and one metastatic. Primary melanocytic lesions, including hyperplasias, benign melanomas, melanomas metastatic to lymph nodes, and melanomas metastatic to nodes and additional visceral organs, were categorized accordingly as types I-IV. Levels of CDKN2A transcripts were most abundant in type III tumor samples and the metastatic cell line but absent in the nonmetastatic cell line. ARF transcripts were expressed in all tumors and cell lines. A UV-signature mutation was detected with the wild-type allele at the CDKN2A locus in type II and III primary tumor samples and in the nonmetastatic cell line. Interestingly, in the metastatic cell line, only the mutant allele was present and expressed. These data suggest dynamic changes in the expression and/or structure of the CDKN2A and ARF genes represent one molecular defect associated with the etiology of melanoma formation and progression in the Monodelphis model system.

Animals↗
PubMed1994

Heterotrimeric GTP-binding proteins (G proteins) and ADP-ribosylation factor (ARF) regulate priming of endosomal membranes for fusion.

An in vitro assay that measures endosome fusion was used to characterize the role of guanosine triphosphate (GTP)-binding proteins in endocytosis. Guanosine 5',3-(thio)triphosphate (GTP gamma S), a nonhydrolyzable analog of GTP, stimulates the binding of cytosolic factors to the endosomal membrane (priming). GTP gamma S also enhances vesicle aggregation, resulting in the formation of an intermediate that is resistant to dilution. In this report we demonstrate that priming precedes the appearance of a dilution-resistant intermediate. Thus, GTP-binding proteins are involved in multiple sequential events preceding endosome fusion. Both heterotrimeric G proteins (G proteins) and ADP-ribosylation factors (ARFs) are GTP-binding proteins that regulate undefined steps involved in endocytosis. The addition of G beta gamma subunits of G proteins to the in vitro fusion assay resulted in inhibition of priming. In contrast, addition of ARF to the assay enhanced priming. Thus, heterotrimeric G proteins and ARF may regulate endocytosis by mediating the binding of cytosolic factor(s) required for fusion to the endosomal membrane. Taken together, the results show that multiple GTP-binding proteins regulate a series of distinct biochemical events required for endosome fusion.

ADP-Ribosylation Factors↗
PubMed2000

Characterization, chromosomal assignment, and tissue expression of a novel human gene belonging to the ARF GAP family.

We have identified and characterized a novel human ADP-ribosylation factor GTPase-activating protein (ARFGAP1) gene that is related to other members of the ARF GAP family. The full-length cDNA for human ARFGAP1 was cloned following the identification of an EST obtained by large-scale cDNA library sequencing through a Blast search of public databases. Structurally, ARFGAP1 encodes a polypeptide of 516 amino acids, which contained a typical GATA-1-type zinc finger motif (CXXCX(16)CXXC) with the four cysteine residues that are highly conserved among other members of the ARF GAP family. The conserved ARF GAP domain may emphasize the biological importance of this gene. The ARFGAP1 gene, which contained 16 exons ranging from 0.5 to 9.3 kb, was mapped to human chromosome 22q13.2-q13.3 using radiation hybridization and in silico analyses. ARFGAP1 is strongly expressed in endocrine glands and testis. Interestingly, the expression of ARFGAP1 in testis is about sixfold higher than that in ovary, indicating a possible role of ARFGAP1 in the physiological function of sperm. Expression of ARFGAP1 in four human fetal tissues and seven cancer cell lines was also detected.

ADP-Ribosylation Factors↗