Characterization of FBX25, encoding a novel brain-expressed F-box protein

Hagens, Olivier; Minina, Eleonora; Schweiger, Susann; Ropers, Hans‐Hilger; Kalscheuer, Vera M.

doi:10.1016/j.bbagen.2005.09.018

Cited by 25 publications

(24 citation statements)

References 33 publications

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“…39 FBX25 protein has been strongly expressed in the human brain, and its disruption has been observed in mentally retarded epileptic-seizure patients. 40 Deletion of the ANKRD15 gene has been reported in a family with parent-of-origin-dependent inheritance of cerebral palsy. 41 Moreover, expression of the ANKRD15 gene has been found to be suppressed in renal cell carcinoma and, thus, has been suggested as a kind of tumor suppressor gene.…”

Section: Discussionmentioning

confidence: 99%

Clinicopathological features and global genomic copy number alterations of pilomyxoid astrocytoma in the hypothalamus/optic pathway: comparative analysis with pilocytic astrocytoma using array-based comparative genomic hybridization

et al. 2008

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Pilomyxoid astrocytoma is a recently identified variant of pilocytic astrocytoma. We studied 11 circumscribed astrocytomas with focal (n ¼ 5) or diffuse (n ¼ 6) pilomyxoid features and compared them with 17 pilocytic astrocytomas from the hypothalamic/chiasmatic region in children. In one patient, a tumor that recurred after initial surgery had changed from pure-form pilomyxoid astrocytoma to the mixed form. The presence of a pilomyxoid area was associated with shorter survival. Next, we compared the comprehensive genome copy number changes in the pilomyxoid astrocytoma (n ¼ 4) with those in pilocytic astrocytoma (n ¼ 6) cases by array-based comparative genomic hybridization. The number of lost clones was larger in pilomyxoid astrocytoma than in pilocytic astrocytoma. Clones located in chromosome 8q24.3 were frequently gained in pilocytic astrocytoma (four of six) and in pilomyxoid astrocytoma (one of four). Clones located in 9p24.3 and 15q26.3 were lost in all of the pilomyxoid astrocytomas and in five of the pilocytic astrocytomas. Those in 8p23.3 showed a copy number loss in three of the pilomyxoid astrocytomas and four of the pilocytic astrocytomas. The frequency of copy number changes was significantly different between pilomyxoid astrocytoma and pilocytic astrocytoma in 47 (3.6%) clones, 20 of them having been located in 2p, 10 in 2q, and 11 in 3q. An unsupervised hierarchical clustering analysis classified the cases into three clusters: one pilomyxoid astrocytoma patient into one cluster, two pilomyxoid astrocytoma patients into another cluster, and six pilocytic astrocytoma patients and one pilomyxoid astrocytoma patient into the third cluster. In conclusion, the presence of mixed-form pilomyxoid astrocytoma, the acquisition of pilocytic astrocytoma features in a recurrent tumor in pure-form pilomyxoid astrocytoma, and the above results of the genome-wide gene copy number analysis suggest that pilomyxoid astrocytoma might be a pathologically and genetically related, aggressive variant of pilocytic astrocytoma with partially different genetic alterations.

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Section: Discussionmentioning

confidence: 99%

Clinicopathological features and global genomic copy number alterations of pilomyxoid astrocytoma in the hypothalamus/optic pathway: comparative analysis with pilocytic astrocytoma using array-based comparative genomic hybridization

et al. 2008

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“…However, the fact that these genes can cooperate to suppress tumorigenesis implies that concomitant loss of multiple genes may create unexpected vulnerabilities not easily revealed through the study of single genes. Thus, codeletion of the 8p TSGs not only might create dependency on Rho signaling (3), but also might deregulate autophagy (15), ubiquitination (16), and other processes. Although the relevant biological effects remain to be determined and are the focus of ongoing work, our results demonstrate that cancer-associated deletions can create phenotypes unique from those arising through loss of a single TSG, and thus should be considered and studied as distinct mutational events.…”

Section: Discussionmentioning

confidence: 99%

A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions

Xue

Kitzing

Roessler

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

135

121

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The large chromosomal deletions frequently observed in cancer genomes are often thought to arise as a "two-hit" mechanism in the process of tumor-suppressor gene (TSG) inactivation. Using a murine model system of hepatocellular carcinoma (HCC) and in vivo RNAi, we test an alternative hypothesis, that such deletions can arise from selective pressure to attenuate the activity of multiple genes. By targeting the mouse orthologs of genes frequently deleted on human 8p22 and adjacent regions, which are lost in approximately half of several other major epithelial cancers, we provide evidence suggesting that multiple genes on chromosome 8p can cooperatively inhibit tumorigenesis in mice, and that their cosuppression can synergistically promote tumor growth. In addition, in human HCC patients, the combined down-regulation of functionally validated 8p TSGs is associated with poor survival, in contrast to the down-regulation of any individual gene. Our data imply that large cancer-associated deletions can produce phenotypes distinct from those arising through loss of a single TSG, and as such should be considered and studied as distinct mutational events.cancer genomics | chromosome 8p deletion | RNAi screen

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“…An F-box protein forms a complex with Skp1, Cul1 and Rbx1 to function as an E3 ubiquitin ligase [13]. Thus, tissue-specific protein degradation may be determined by an F- box protein bioavailability.…”

Section: Discussionmentioning

confidence: 99%

“…1 and 3). It is reported that Fbxo25 is expressed in the adult heart, brain, liver and kidney [13]. Thus, Fbxo25 expression should be tightly regulated to prevent cardiac transcription factors from untimely degradation.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Fbxo25 controls Tbx5 and Nkx2–5 transcriptional activity to regulate cardiomyocyte development

Jeong

Jung

Sim

et al. 2015

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

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Characterization of FBX25, encoding a novel brain-expressed F-box protein

Cited by 25 publications

References 33 publications

Clinicopathological features and global genomic copy number alterations of pilomyxoid astrocytoma in the hypothalamus/optic pathway: comparative analysis with pilocytic astrocytoma using array-based comparative genomic hybridization

Clinicopathological features and global genomic copy number alterations of pilomyxoid astrocytoma in the hypothalamus/optic pathway: comparative analysis with pilocytic astrocytoma using array-based comparative genomic hybridization

A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions

Fbxo25 controls Tbx5 and Nkx2–5 transcriptional activity to regulate cardiomyocyte development

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