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Fusion gene ID: 27690 |
FusionGeneSummary for PLK3_PLK3 |
 Fusion gene summary |
| Fusion gene information | Fusion gene name: PLK3_PLK3 | Fusion gene ID: 27690 | Hgene | Tgene | Gene symbol | PLK3 | PLK3 | Gene ID | 1263 | 1263 |
| Gene name | polo like kinase 3 | polo like kinase 3 | |
| Synonyms | CNK|FNK|PLK-3|PRK | CNK|FNK|PLK-3|PRK | |
| Cytomap | 1p34.1 | 1p34.1 | |
| Type of gene | protein-coding | protein-coding | |
| Description | serine/threonine-protein kinase PLK3FGF-inducible kinasecytokine-inducible serine/threonine-protein kinaseproliferation-related kinase | serine/threonine-protein kinase PLK3FGF-inducible kinasecytokine-inducible serine/threonine-protein kinaseproliferation-related kinase | |
| Modification date | 20180519 | 20180519 | |
| UniProtAcc | Q9H4B4 | Q9H4B4 | |
| Ensembl transtripts involved in fusion gene | ENST00000372201, ENST00000465443, | ENST00000372201, ENST00000465443, | |
| Fusion gene scores | * DoF score | 1 X 1 X 1=1 | 2 X 2 X 1=4 |
| # samples | 1 | 2 | |
| ** MAII score | log2(1/1*10)=3.32192809488736 | log2(2/4*10)=2.32192809488736 | |
| Context | PubMed: PLK3 [Title/Abstract] AND PLK3 [Title/Abstract] AND fusion [Title/Abstract] | ||
| Functional or gene categories assigned by FusionGDB annotation | |||
| * DoF score (Degree of Frequency) = # partners X # break points X # cancer types ** MAII score (Major Active Isofusion Index) = log2(# samples/DoF score*10) |
| Gene ontology of each fusion partner gene with evidence of Inferred from Direct Assay (IDA) from Entrez |
| Partner | Gene | GO ID | GO term | PubMed ID |
| Hgene | PLK3 | GO:0000122 | negative regulation of transcription by RNA polymerase II | 19490146 |
| Hgene | PLK3 | GO:0000302 | response to reactive oxygen species | 11447225 |
| Hgene | PLK3 | GO:0006970 | response to osmotic stress | 21098032 |
| Hgene | PLK3 | GO:0006974 | cellular response to DNA damage stimulus | 19490146 |
| Hgene | PLK3 | GO:0009314 | response to radiation | 21376736 |
| Hgene | PLK3 | GO:0043066 | negative regulation of apoptotic process | 19490146 |
| Hgene | PLK3 | GO:0051302 | regulation of cell division | 20951827 |
| Hgene | PLK3 | GO:0090166 | Golgi disassembly | 14980500|19103756 |
| Hgene | PLK3 | GO:1904716 | positive regulation of chaperone-mediated autophagy | 27344333 |
| Hgene | PLK3 | GO:2000777 | positive regulation of proteasomal ubiquitin-dependent protein catabolic process involved in cellular response to hypoxia | 20889502 |
| Tgene | PLK3 | GO:0000122 | negative regulation of transcription by RNA polymerase II | 19490146 |
| Tgene | PLK3 | GO:0000302 | response to reactive oxygen species | 11447225 |
| Tgene | PLK3 | GO:0006970 | response to osmotic stress | 21098032 |
| Tgene | PLK3 | GO:0006974 | cellular response to DNA damage stimulus | 19490146 |
| Tgene | PLK3 | GO:0009314 | response to radiation | 21376736 |
| Tgene | PLK3 | GO:0043066 | negative regulation of apoptotic process | 19490146 |
| Tgene | PLK3 | GO:0051302 | regulation of cell division | 20951827 |
| Tgene | PLK3 | GO:0090166 | Golgi disassembly | 14980500|19103756 |
| Tgene | PLK3 | GO:1904716 | positive regulation of chaperone-mediated autophagy | 27344333 |
| Tgene | PLK3 | GO:2000777 | positive regulation of proteasomal ubiquitin-dependent protein catabolic process involved in cellular response to hypoxia | 20889502 |
| Fusion gene information from three resources (ChiTars (NAR, 2018), tumorfusions (NAR, 2018), Gao et al. (Cell, 2018)) * All genome coordinats were lifted-over on hg19. * Click on the break point to see the gene structure around the break point region using the UCSC Genome Browser. |
| Data type | Source | Cancer type | Sample | Hgene | Hchr | Hbp | Hstrand | Tgene | Tchr | Tbp | Tstrand |
| ChiTaRS3.1 | BQ300580 | PLK3 | chr1 | 45271046 | + | PLK3 | chr1 | 45268728 | + |
| * LD: Li Ding group's fusion gene list RV: Roel Verhaak group's fusion gene list ChiTaRs fusion database |
| Open reading frame (ORF) analsis of fusion genes based on Ensembl gene isoform structure. * Click on the break point to see the gene structure around the break point region using the UCSC Genome Browser. |
| ORF | Henst | Tenst | Hgene | Hchr | Hbp | Hstrand | Tgene | Tchr | Tbp | Tstrand |
| Frame-shift | ENST00000372201 | ENST00000372201 | PLK3 | chr1 | 45271046 | + | PLK3 | chr1 | 45268728 | + |
| 5CDS-3UTR | ENST00000372201 | ENST00000465443 | PLK3 | chr1 | 45271046 | + | PLK3 | chr1 | 45268728 | + |
| 3UTR-3CDS | ENST00000465443 | ENST00000372201 | PLK3 | chr1 | 45271046 | + | PLK3 | chr1 | 45268728 | + |
| 3UTR-3UTR | ENST00000465443 | ENST00000465443 | PLK3 | chr1 | 45271046 | + | PLK3 | chr1 | 45268728 | + |
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FusionProtFeatures for PLK3_PLK3 |
| Main function of each fusion partner protein. (from UniProt) |
| Hgene | Tgene |
| PLK3 | PLK3 |
| Serine/threonine-protein kinase involved in cell cycleregulation, response to stress and Golgi disassembly. Polo-likekinases act by binding and phosphorylating proteins are thatalready phosphorylated on a specific motif recognized by the POLObox domains. Phosphorylates ATF2, BCL2L1, CDC25A, CDC25C, CHEK2,HIF1A, JUN, p53/TP53, p73/TP73, PTEN, TOP2A and VRK1. Involved incell cycle regulation: required for entry into S phase andcytokinesis. Phosphorylates BCL2L1, leading to regulate the G2checkpoint and progression to cytokinesis during mitosis. Plays akey role in response to stress: rapidly activated upon stressstimulation, such as ionizing radiation, reactive oxygen species(ROS), hyperosmotic stress, UV irradiation and hypoxia. Involvedin DNA damage response and G1/S transition checkpoint byphosphorylating CDC25A, p53/TP53 and p73/TP73. Phosphorylatesp53/TP53 in response to reactive oxygen species (ROS), therebypromoting p53/TP53-mediated apoptosis. Phosphorylates CHEK2 inresponse to DNA damage, promoting the G2/M transition checkpoint.Phosphorylates the transcription factor p73/TP73 in response toDNA damage, leading to inhibit p73/TP73-mediated transcriptionalactivation and pro-apoptotic functions. Phosphorylates HIF1A andJUN is response to hypoxia. Phosphorylates ATF2 followinghyperosmotic stress in corneal epithelium. Also involved in Golgidisassembly during the cell cycle: part of a MEK1/MAP2K1-dependentpathway that induces Golgi fragmentation during mitosis bymediating phosphorylation of VRK1. May participate in endomitoticcell cycle, a form of mitosis in which both karyokinesis andcytokinesis are interrupted and is a hallmark of megakaryocytedifferentiation, via its interaction with CIB1.{ECO:0000269|PubMed:10557092, ECO:0000269|PubMed:11156373,ECO:0000269|PubMed:11447225, ECO:0000269|PubMed:11551930,ECO:0000269|PubMed:11971976, ECO:0000269|PubMed:12242661,ECO:0000269|PubMed:14968113, ECO:0000269|PubMed:14980500,ECO:0000269|PubMed:15021912, ECO:0000269|PubMed:16478733,ECO:0000269|PubMed:16481012, ECO:0000269|PubMed:17264206,ECO:0000269|PubMed:17804415, ECO:0000269|PubMed:18062778,ECO:0000269|PubMed:18650425, ECO:0000269|PubMed:19103756,ECO:0000269|PubMed:19490146, ECO:0000269|PubMed:20889502,ECO:0000269|PubMed:20940307, ECO:0000269|PubMed:20951827,ECO:0000269|PubMed:21098032, ECO:0000269|PubMed:21264284,ECO:0000269|PubMed:21376736, ECO:0000269|PubMed:21840391,ECO:0000269|PubMed:9353331}. | Serine/threonine-protein kinase involved in cell cycleregulation, response to stress and Golgi disassembly. Polo-likekinases act by binding and phosphorylating proteins are thatalready phosphorylated on a specific motif recognized by the POLObox domains. Phosphorylates ATF2, BCL2L1, CDC25A, CDC25C, CHEK2,HIF1A, JUN, p53/TP53, p73/TP73, PTEN, TOP2A and VRK1. Involved incell cycle regulation: required for entry into S phase andcytokinesis. Phosphorylates BCL2L1, leading to regulate the G2checkpoint and progression to cytokinesis during mitosis. Plays akey role in response to stress: rapidly activated upon stressstimulation, such as ionizing radiation, reactive oxygen species(ROS), hyperosmotic stress, UV irradiation and hypoxia. Involvedin DNA damage response and G1/S transition checkpoint byphosphorylating CDC25A, p53/TP53 and p73/TP73. Phosphorylatesp53/TP53 in response to reactive oxygen species (ROS), therebypromoting p53/TP53-mediated apoptosis. Phosphorylates CHEK2 inresponse to DNA damage, promoting the G2/M transition checkpoint.Phosphorylates the transcription factor p73/TP73 in response toDNA damage, leading to inhibit p73/TP73-mediated transcriptionalactivation and pro-apoptotic functions. Phosphorylates HIF1A andJUN is response to hypoxia. Phosphorylates ATF2 followinghyperosmotic stress in corneal epithelium. Also involved in Golgidisassembly during the cell cycle: part of a MEK1/MAP2K1-dependentpathway that induces Golgi fragmentation during mitosis bymediating phosphorylation of VRK1. May participate in endomitoticcell cycle, a form of mitosis in which both karyokinesis andcytokinesis are interrupted and is a hallmark of megakaryocytedifferentiation, via its interaction with CIB1.{ECO:0000269|PubMed:10557092, ECO:0000269|PubMed:11156373,ECO:0000269|PubMed:11447225, ECO:0000269|PubMed:11551930,ECO:0000269|PubMed:11971976, ECO:0000269|PubMed:12242661,ECO:0000269|PubMed:14968113, ECO:0000269|PubMed:14980500,ECO:0000269|PubMed:15021912, ECO:0000269|PubMed:16478733,ECO:0000269|PubMed:16481012, ECO:0000269|PubMed:17264206,ECO:0000269|PubMed:17804415, ECO:0000269|PubMed:18062778,ECO:0000269|PubMed:18650425, ECO:0000269|PubMed:19103756,ECO:0000269|PubMed:19490146, ECO:0000269|PubMed:20889502,ECO:0000269|PubMed:20940307, ECO:0000269|PubMed:20951827,ECO:0000269|PubMed:21098032, ECO:0000269|PubMed:21264284,ECO:0000269|PubMed:21376736, ECO:0000269|PubMed:21840391,ECO:0000269|PubMed:9353331}. |
| Retention analysis result of each fusion partner protein across 39 protein features of UniProt such as six molecule processing features, 13 region features, four site features, six amino acid modification features, two natural variation features, five experimental info features, and 3 secondary structure features. Here, because of limited space for viewing, we only show the protein feature retention information belong to the 13 regional features. All retention annotation result can be downloaded at . * Minus value of BPloci means that the break pointn is located before the CDS. |
| - In-frame and retained protein feature among the 13 regional features. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Protein feature | Protein feature note |
| - In-frame and not-retained protein feature among the 13 regional features. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Protein feature | Protein feature note |
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FusionGeneSequence for PLK3_PLK3 |
| For in-frame fusion transcripts, we provide the fusion transcript sequences and fusion amino acid sequences. (nt: nucleotides, aa: amino acids) |
| * Fusion amino acid sequences. |
| * Fusion transcript sequences (only coding sequence (CDS) region). |
| * Fusion transcript sequences (Full-length transcript). |
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FusionGenePPI for PLK3_PLK3 |
| Go to ChiPPI (Chimeric Protein-Protein interactions) to see the chimeric PPI interaction in . |
| Protein-protein interactors with each fusion partner protein in wild-type (BIOGRID-3.4.160) |
| Hgene | Hgene's interactors | Tgene | Tgene's interactors |
| - Retained PPIs in in-frame fusion. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Still interaction with |
| - Lost PPIs in in-frame fusion. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Interaction lost with |
| - Retained PPIs, but lost function due to frame-shift fusion. |
| Partner | Gene | Hbp | Tbp | ENST | Strand | BPexon | TotalExon | Protein feature loci | *BPloci | TotalLen | Interaction lost with |
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RelatedDrugs for PLK3_PLK3 |
| Drugs targeting genes involved in this fusion gene. (DrugBank Version 5.1.0 2018-04-02) |
| Partner | Gene | UniProtAcc | DrugBank ID | Drug name | Drug activity | Drug type | Drug status |
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RelatedDiseases for PLK3_PLK3 |
| Diseases associated with fusion partners. (DisGeNet 4.0) |
| Partner | Gene | Disease ID | Disease name | # pubmeds | Source |
Copyright 2018-Present -The University of Texas Health Science Center at Houston (UTHealth)
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