UTHEALTH HOME    ABOUT SBMI    A-Z    WEBMAIL    INSIDE THE UNIVERSITY
FusionGDB Logo

Home

Download

Statistics

Examples

Help

Contact

Terms of Use

Center for Computational Systems Medicine
leaf

Kinase Fusion Gene Summary

leaf

Kinase Fusion Gene Sample Information

leaf

Kinase Fusion ORF Analysis

leaf

Kinase Fusion Amino Acid Sequences

leaf

Multiple Sequence Alignment of All Fusion Protein Isoforms

leaf

Kinase Fusion Protein Functional Features

leaf

Kinase Fusion Protein Structures

leaf

Comparison of Fusion Protein Isoforms

leaf

Comparison of Fusion Protein Sequences/Structures with Known Sequences/Structures from PDB

leaf

pLDDT Scores and Difference Analysis of pLDDT Scores Between the Active Sites (Best) and Non-Active Sites.

leaf

Ramachandran Plot of Kinase Fusion Protein Structure

leaf

Potential Active Site Information

leaf

Virtual Screening Results

leaf

Kinase-Substrate Information

leaf

Related Drugs with This Kinase Fusion Protein

leaf

Related Disease with This Kinase Fusion Protein

leaf

Clinical Trials of the Found Drugs/Small Molecules

Kinase Fusion Gene:PER1_IKBKB

Kinase Fusion Protein Summary

check button Kinase Fusion gene summary
Kinase Fusion partner gene informationKinase Fusion gene name: PER1_IKBKB
KinaseFusionDB ID: KFG4621
FusionGDB2.0 ID: KFG4621
HgeneTgene
Gene symbol

PER1

IKBKB

Gene ID

5187

3551

Gene nameperiod circadian regulator 1inhibitor of nuclear factor kappa B kinase subunit beta
SynonymsPER|RIGUI|hPERIKK-2|IKK-beta|IKK2|IKKB|IMD15|IMD15A|IMD15B|NFKBIKB
Cytomap

17p13.1

8p11.21

Type of geneprotein-codingprotein-coding
Descriptionperiod circadian protein homolog 1Period, drosophila, homolog ofcircadian clock protein PERIOD 1circadian pacemaker protein RIGUIhPER1period circadian clock 1period homolog 1inhibitor of nuclear factor kappa-B kinase subunit betaI-kappa-B kinase 2I-kappa-B-kinase betainhibitor of kappa light polypeptide gene enhancer in B-cells, kinase betanuclear factor NF-kappa-B inhibitor kinase betanuclear factor kappa B kinase subun
Modification date2024040720240407
UniProtAcc

O15534

O14920

Ensembl transtripts involved in fusion geneENST idsENST00000317276, ENST00000354903, 
ENST00000578089, ENST00000581082, 
ENST00000379708, ENST00000416505, 
ENST00000518983, ENST00000519735, 
ENST00000520810, ENST00000520835, 
ENST00000522147, ENST00000522785, 
Context (manual curation of fusion genes in KinaseFusionDB)

PubMed: PER1 [Title/Abstract] AND IKBKB [Title/Abstract] AND fusion [Title/Abstract]

Most frequent breakpoint (based on all fusion genes of FusionGDB 2.0)PER1(7870321)-IKBKB(42183128), # samples:1
check button Gene ontology of each fusion partner gene with evidence of Inferred from Direct Assay (IDA) from Entrez
PartnerGeneGO IDGO termPubMed ID
HgenePER1

GO:0032922

circadian regulation of gene expression

18411297|24005054

TgeneIKBKB

GO:0006468

protein phosphorylation

15084260|20434986

TgeneIKBKB

GO:0007249

canonical NF-kappaB signal transduction

9346484

TgeneIKBKB

GO:0018105

peptidyl-serine phosphorylation

21399639|25326418

TgeneIKBKB

GO:0042325

regulation of phosphorylation

26212789

TgeneIKBKB

GO:0043123

positive regulation of canonical NF-kappaB signal transduction

9346484

TgeneIKBKB

GO:0045944

positive regulation of transcription by RNA polymerase II

23091055|23453807

TgeneIKBKB

GO:0051092

positive regulation of NF-kappaB transcription factor activity

15790681

TgeneIKBKB

GO:0051604

protein maturation

11297557

TgeneIKBKB

GO:0071356

cellular response to tumor necrosis factor

23091055


check buttonKinase Fusion gene breakpoints across PER1 (5'-gene)
* Click on the image to open the UCSC genome browser with custom track showing this image in a new window.

check buttonKinase Fusion gene breakpoints across IKBKB (3'-gene)
* Click on the image to open the UCSC genome browser with custom track showing this image in a new window.


Top

Kinase Fusion Gene Sample Information

check buttonKinase Fusion gene information.
check button Kinase Fusion gene information from four resources (ChiTars 5.0, ChimerDB 4.0, COSMIC, and CCLE)
* 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.
SourceSampleHgeneHchrHbpTgeneTchrTbp
ChiTaRS5.0BC110917PER1chr17

7870321

IKBKBchr8

42183128



Top

Kinase Fusion ORF Analysis


check buttonKinase Fusion information from ORFfinder translation from full-length transcript sequence from KinaseFusionDB.
HenstTenstHgeneHchrHbpTgeneTchrTbpSeq length
(transcript)
Seq length
(amino acids)

Top

Kinase Fusion Amino Acid Sequences


check button For individual full-length fusion transcript sequence from KinaseFusionDB, we ran ORFfinder and chose the longest ORF among the all predicted ones.
>Henst_Tenst_Hgene_Hchr_Hbp_Tgene_Tchr_Tbp_length(fusion AA)_AAseq

Multiple Sequence Alignment of All Fusion Protein Isoforms



Top

Kinase Fusion Protein Functional Features


check button Four levels of functional features of fusion genes
Go to FGviewer search page for the most frequent breakpoint (https://ccsmweb.uth.edu/FGviewer/:7870321/:42183128)
- FGviewer provides the online visualization of the retention search of the protein functional features across DNA, RNA, protein, and pathological levels.
- How to search
1. Put your fusion gene symbol.
2. Press the tab key until there will be shown the breakpoint information filled.
4. Go down and press 'Search' tab twice.
4. Go down to have the hyperlink of the search result.
5. Click the hyperlink.
6. See the FGviewer result for your fusion gene.
FGviewer

check buttonMain function of each fusion partner protein. (from UniProt)
HgeneTgene
PER1

O15534

IKBKB

O14920

FUNCTION: Transcriptional repressor which forms a core component of the circadian clock. The circadian clock, an internal time-keeping system, regulates various physiological processes through the generation of approximately 24 hour circadian rhythms in gene expression, which are translated into rhythms in metabolism and behavior. It is derived from the Latin roots 'circa' (about) and 'diem' (day) and acts as an important regulator of a wide array of physiological functions including metabolism, sleep, body temperature, blood pressure, endocrine, immune, cardiovascular, and renal function. Consists of two major components: the central clock, residing in the suprachiasmatic nucleus (SCN) of the brain, and the peripheral clocks that are present in nearly every tissue and organ system. Both the central and peripheral clocks can be reset by environmental cues, also known as Zeitgebers (German for 'timegivers'). The predominant Zeitgeber for the central clock is light, which is sensed by retina and signals directly to the SCN. The central clock entrains the peripheral clocks through neuronal and hormonal signals, body temperature and feeding-related cues, aligning all clocks with the external light/dark cycle. Circadian rhythms allow an organism to achieve temporal homeostasis with its environment at the molecular level by regulating gene expression to create a peak of protein expression once every 24 hours to control when a particular physiological process is most active with respect to the solar day. Transcription and translation of core clock components (CLOCK, NPAS2, BMAL1, BMAL2, PER1, PER2, PER3, CRY1 and CRY2) plays a critical role in rhythm generation, whereas delays imposed by post-translational modifications (PTMs) are important for determining the period (tau) of the rhythms (tau refers to the period of a rhythm and is the length, in time, of one complete cycle). A diurnal rhythm is synchronized with the day/night cycle, while the ultradian and infradian rhythms have a period shorter and longer than 24 hours, respectively. Disruptions in the circadian rhythms contribute to the pathology of cardiovascular diseases, cancer, metabolic syndromes and aging. A transcription/translation feedback loop (TTFL) forms the core of the molecular circadian clock mechanism. Transcription factors, CLOCK or NPAS2 and BMAL1 or BMAL2, form the positive limb of the feedback loop, act in the form of a heterodimer and activate the transcription of core clock genes and clock-controlled genes (involved in key metabolic processes), harboring E-box elements (5'-CACGTG-3') within their promoters. The core clock genes: PER1/2/3 and CRY1/2 which are transcriptional repressors form the negative limb of the feedback loop and interact with the CLOCK|NPAS2-BMAL1|BMAL2 heterodimer inhibiting its activity and thereby negatively regulating their own expression. This heterodimer also activates nuclear receptors NR1D1/2 and RORA/B/G, which form a second feedback loop and which activate and repress BMAL1 transcription, respectively. Regulates circadian target genes expression at post-transcriptional levels, but may not be required for the repression at transcriptional level. Controls PER2 protein decay. Represses CRY2 preventing its repression on CLOCK/BMAL1 target genes such as FXYD5 and SCNN1A in kidney and PPARA in liver. Besides its involvement in the maintenance of the circadian clock, has an important function in the regulation of several processes. Participates in the repression of glucocorticoid receptor NR3C1/GR-induced transcriptional activity by reducing the association of NR3C1/GR to glucocorticoid response elements (GREs) by BMAL1:CLOCK. Plays a role in the modulation of the neuroinflammatory state via the regulation of inflammatory mediators release, such as CCL2 and IL6. In spinal astrocytes, negatively regulates the MAPK14/p38 and MAPK8/JNK MAPK cascades as well as the subsequent activation of NFkappaB. Coordinately regulates the expression of multiple genes that are involved in the regulation of renal sodium reabsorption. Can act as gene expression activator in a gene and tissue specific manner, in kidney enhances WNK1 and SLC12A3 expression in collaboration with CLOCK. Modulates hair follicle cycling. Represses the CLOCK-BMAL1 induced transcription of BHLHE40/DEC1. {ECO:0000269|PubMed:24005054}.FUNCTION: Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses (PubMed:20434986, PubMed:20797629, PubMed:21138416, PubMed:9346484, PubMed:30337470). Acts as a part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation (PubMed:9346484). Phosphorylates inhibitors of NF-kappa-B on 2 critical serine residues (PubMed:9346484, PubMed:20434986, PubMed:20797629, PubMed:21138416). These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome (PubMed:9346484, PubMed:20434986, PubMed:20797629, PubMed:21138416). In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis (PubMed:9346484, PubMed:20434986, PubMed:20797629, PubMed:21138416). In addition to the NF-kappa-B inhibitors, phosphorylates several other components of the signaling pathway including NEMO/IKBKG, NF-kappa-B subunits RELA and NFKB1, as well as IKK-related kinases TBK1 and IKBKE (PubMed:11297557, PubMed:14673179, PubMed:20410276, PubMed:21138416). IKK-related kinase phosphorylations may prevent the overproduction of inflammatory mediators since they exert a negative regulation on canonical IKKs (PubMed:11297557, PubMed:20410276, PubMed:21138416). Phosphorylates FOXO3, mediating the TNF-dependent inactivation of this pro-apoptotic transcription factor (PubMed:15084260). Also phosphorylates other substrates including NAA10, NCOA3, BCL10 and IRS1 (PubMed:19716809, PubMed:17213322). Phosphorylates RIPK1 at 'Ser-25' which represses its kinase activity and consequently prevents TNF-mediated RIPK1-dependent cell death (By similarity). Phosphorylates the C-terminus of IRF5, stimulating IRF5 homodimerization and translocation into the nucleus (PubMed:25326418). {ECO:0000250|UniProtKB:O88351, ECO:0000269|PubMed:11297557, ECO:0000269|PubMed:14673179, ECO:0000269|PubMed:15084260, ECO:0000269|PubMed:17213322, ECO:0000269|PubMed:19716809, ECO:0000269|PubMed:20410276, ECO:0000269|PubMed:20434986, ECO:0000269|PubMed:20797629, ECO:0000269|PubMed:21138416, ECO:0000269|PubMed:25326418, ECO:0000269|PubMed:30337470, ECO:0000269|PubMed:9346484}.

check buttonRetention 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

download page

* Minus value of BPloci means that the break pointn is located before the CDS.

check button - Retained domain in the 5'-partner of fusion protein (protein functional feature from UniProt).
PartnerHgeneeneHbpTgeneeneTbpENSTBPexonTotalExonProtein feature lociBPlociTotalLenFeatureNote


check button - Retained domain in the 3'-partner of fusion protein (protein functional feature from UniProt).
PartnerHgeneeneHbpTgeneeneTbpENSTBPexonTotalExonProtein feature lociBPlociTotalLenFeatureNote


Top

Kinase-Substrate Information of PER1_IKBKB


check button Phosphorylation target of the kinase
(phosphosite, 03-17-2024)
KinaseKinase UniProt AccKinase speciesSubstrateSubstrate UniProt AccSubstrate phosphorylated residuesSubstrate phosphorylated sites (+/-7AA)Domain
IKBKBO14920humanCYLDQ9NQC7S432KMPNTNGsIGHsPLsCYLD_phos_site
IKBKBO14920humanBBC3Q9BXH1S106LAEQHLEsPVPSAPGPUMA
IKBKBO14920humanNFKB1P19838S923DELRDSDsVCDsGVE
IKBKBO14920humanIRF3Q14653T404NsHPLsLtsDQYKAY
IKBKBO14920humanFOSP01100S308ADWEPLHsGSLGMGP
IKBKBO14920humanCOPS5Q92905S201kPPDEGPsEyQtIPL
IKBKBO14920humanTP63Q9H3D4S43yRSTMSQsTQtNEFL
IKBKBO14920humanTSC1Q92574S487AAIsRELsEItTAEAHamartin
IKBKBO14920humanBCL10O95999S138NNLsRsNsDEsNFsE
IKBKBO14920humanTNFRSF1AP19438S381FVRRLGLsDHEIDRLDeath
IKBKBO14920humanCYLDQ9NQC7S439sIGHsPLsLsAQsVMCYLD_phos_site
IKBKBO14920humanBBC3Q9BXH1S96RPDGPQPsLSLAEQHPUMA
IKBKBO14920humanTNFAIP3P21580S381EPsVPQLsLMDVKCE
IKBKBO14920humanRAPGEF2Q9Y4G8S1254GsWTSCSsGsHDNIQ
IKBKBO14920humanMTURNQ8N3F0S58GDNFHVWsESEDCLPDUF4581
IKBKBO14920humanCYLDQ9NQC7S436TNGsIGHsPLsLsAQCYLD_phos_site
IKBKBO14920humanIRF3Q14653S398VDLHIsNsHPLsLts
IKBKBO14920humanIKBKGQ9Y6K9S43PAMLHLPsEQGAPEt
IKBKBO14920humanIKBKGQ9Y6K9S68LRDAIRQsNQILRERNEMO
IKBKBO14920humanRELAQ04206S536sGDEDFSsIADMDFS
IKBKBO14920humanMAVSQ7Z434S442CFEDLAIsASTSLGM
IKBKBO14920humanRELAQ04206S468AVFTDLAsVDNsEFQ
IKBKBO14920humanDOK1Q99704S450sHNsALysQVQKSGA
IKBKBO14920humanEDC4Q6P2E9S583PAPADFLsLssEtKP
IKBKBO14920humanBCL10O95999S136AtNNLsRsNsDEsNF
IKBKBO14920humanPFKFB3Q16875S269QGRIGGDsGLSsRGKHis_Phos_1
IKBKBO14920humanBCL3P20749S454PsPAPGGs_______
IKBKBO14920humanASB8Q9H765S31RTIAAIRsFPHDNVEAnk_2
IKBKBO14920humanBCL10O95999S144NsDEsNFsEkLRAST
IKBKBO14920humanTSC1Q92574S511DsPFyRDsLPGsQRKHamartin
IKBKBO14920humanRPS3P23396S209kPLPDHVsIVEPkDE
IKBKBO14920humanHTTP42858S16kAFEsLksFQQQQQQ
IKBKBO14920humanIRF3Q14653S402IsNsHPLsLtsDQYK
IKBKBO14920humanIKBKBO14920S258GTVKFsssLPyPNNLPkinase
IKBKBO14920humanOPTNQ96CV9S513FEDGGRQsLMEMQsR
IKBKBO14920humanMYCP01106S82PLsPsRRsGLCsPSyMyc_N
IKBKBO14920humanCOPS5Q92905T205EGPsEyQtIPLNkIE
IKBKBO14920humanRELAQ04206S311RtyEtFksIMkksPF
IKBKBO14920humanRELAQ04206S42RYkCEGRsAGsIPGERHD_DNA_bind
IKBKBO14920humanNFKBIAP25963S32LLDDRHDsGLDsMkD
IKBKBO14920humanIKBKGQ9Y6K9S85ELLHFQAsQREEKEFNEMO
IKBKBO14920humanFOXO3O43524S644GLDFNFDsLISTQNVFOXO-TAD
IKBKBO14920humanRELQ04864S557SNTTVFVsQSDAFEG
IKBKBO14920humanIRF5Q13568S446DsIRLQIsNPDLKDR
IKBKBO14920humanNFKB1P19838S927DSDsVCDsGVETsFR
IKBKBO14920humanDOK1Q99704S446sGIKsHNsALysQVQ
IKBKBO14920humanCYLDQ9NQC7S441GHsPLsLsAQsVMEECYLD_phos_site
IKBKBO14920humanRELAQ04206S131RDLEQAIsQRIQtNNRHD_DNA_bind
IKBKBO14920humanMYCP01106S86sRRsGLCsPSyVAVtMyc_N
IKBKBO14920humanRELAQ04206S45CEGRsAGsIPGERSTRHD_DNA_bind
IKBKBO14920humanTP73O15350S471GEMSSSHsAQSMVSG
IKBKBO14920humanTP63Q9H3D4S51TQtNEFLsPEVFQHI
IKBKBO14920humanRELAQ04206S261tPPYADPsLQAPVRVRHD_dimer
IKBKBO14920humanDOK1Q99704S439EPGtATGsGIKsHNs
IKBKBO14920humanNFKBIAP25963S36RHDsGLDsMkDEEyE
IKBKBO14920humanRELBQ01201S472DFFSGTVsLPGLEPPRelB_transactiv
IKBKBO14920humanTMIGD2Q96BF3S220GKDQRGQsIyStSFP
IKBKBO14920humanNFKB1P19838S80sSEKNKKsYPQVKICRHD_DNA_bind
IKBKBO14920humanHTTP42858S13kLMkAFEsLksFQQQ
IKBKBO14920humanEDC4Q6P2E9S855GLQEKHKsLAFHRPP
IKBKBO14920humanCDKN2AP42771S8MEPAAGssMEPSADW
IKBKBO14920humanIRF3Q14653S396NtVDLHIsNsHPLsL
IKBKBO14920humanIKBKGQ9Y6K9S31QDVLGEEsPLGKPAM
IKBKBO14920humanCYLDQ9NQC7S568LAFGGYLsEVVEENT
IKBKBO14920humanEDC4Q6P2E9S107IVASsDssISskARG
IKBKBO14920humanFOXO1Q12778S319TFRPRtssNAstIsG
IKBKBO14920humanSTAT1P42224T749EFDsMMNtV______
IKBKBO14920humanCYLDQ9NQC7S444PLsLsAQsVMEELNTCYLD_phos_site
IKBKBO14920humanCYLDQ9NQC7S422RFHsLPFsLtKMPNTCYLD_phos_site
IKBKBO14920humanBBC3Q9BXH1S10RARQEGSsPEPVEGLPUMA
IKBKBO14920humanEDC4Q6P2E9S405PDIFSSVsVPPSLKVGe1_WD40
IKBKBO14920humanBCL10O95999S141sRsNsDEsNFsEkLR
IKBKBO14920humanIRS1P35568S312tEsItAtsPAsMVGG
IKBKBO14920humanIKBKBO14920S177AkELDQGsLCtsFVGPkinase
IKBKBO14920humanIKBKBO14920S181DQGsLCtsFVGTLQyPkinase
IKBKBO14920humanIKBKGQ9Y6K9S376PPAPAyLssPLALPs
IKBKBO14920humanCYLDQ9NQC7S418TTENRFHsLPFsLtKCYLD_phos_site
IKBKBO14920humanNFKB1P19838S932CDsGVETsFRKLsFt
IKBKBO14920humanHTTP42858T3_____MAtLEkLMkA
IKBKBO14920humanSNAP23O00161S95NRTkNFEsGkAykTtSNAP-25
IKBKBO14920humanBCL10O95999S134DGAtNNLsRsNsDEs
IKBKBO14920humanDOK1Q99704S443ATGsGIKsHNsALys
IKBKBO14920humanIRF3Q14653S405sHPLsLtsDQYKAYL


check button Biological Network Integration of This Kinase and Substrates
(GeneMANIA website)

check button Enriched GO biological processes of the phosphorylation target genes of the kinase
KinaseGOIDGO termP.adjust
IKBKBIDDescription0.00e+00
IKBKBGO:0007249canonical NF-kappaB signal transduction1.34e-14
IKBKBGO:0051090regulation of DNA-binding transcription factor activity4.75e-10
IKBKBGO:0071356cellular response to tumor necrosis factor4.95e-10
IKBKBGO:0034612response to tumor necrosis factor9.33e-10
IKBKBGO:0043122regulation of canonical NF-kappaB signal transduction9.58e-10
IKBKBGO:0033209tumor necrosis factor-mediated signaling pathway1.28e-08
IKBKBGO:0002757immune response-activating signaling pathway1.87e-08
IKBKBGO:0002764immune response-regulating signaling pathway3.11e-08
IKBKBGO:0038061non-canonical NF-kappaB signal transduction8.61e-08
IKBKBGO:0043123positive regulation of canonical NF-kappaB signal transduction6.12e-07
IKBKBGO:0032479regulation of type I interferon production6.12e-07
IKBKBGO:0032606type I interferon production6.12e-07
IKBKBGO:0050851antigen receptor-mediated signaling pathway7.86e-07
IKBKBGO:0009612response to mechanical stimulus9.86e-07
IKBKBGO:0009615response to virus1.06e-06
IKBKBGO:0002429immune response-activating cell surface receptor signaling pathway1.06e-06
IKBKBGO:0002753cytosolic pattern recognition receptor signaling pathway1.43e-06
IKBKBGO:0002221pattern recognition receptor signaling pathway1.70e-06
IKBKBGO:0032088negative regulation of NF-kappaB transcription factor activity1.70e-06
IKBKBGO:0002768immune response-regulating cell surface receptor signaling pathway1.76e-06
IKBKBGO:0031349positive regulation of defense response2.01e-06
IKBKBGO:0050862positive regulation of T cell receptor signaling pathway2.42e-06
IKBKBGO:0002758innate immune response-activating signaling pathway2.44e-06
IKBKBGO:0002218activation of innate immune response4.31e-06
IKBKBGO:2001233regulation of apoptotic signaling pathway4.68e-06
IKBKBGO:0032495response to muramyl dipeptide5.13e-06
IKBKBGO:0032608interferon-beta production6.80e-06
IKBKBGO:0032648regulation of interferon-beta production6.80e-06
IKBKBGO:0032727positive regulation of interferon-alpha production8.13e-06
IKBKBGO:0035994response to muscle stretch9.29e-06
IKBKBGO:2000630positive regulation of miRNA metabolic process9.29e-06
IKBKBGO:0097193intrinsic apoptotic signaling pathway9.81e-06
IKBKBGO:0050857positive regulation of antigen receptor-mediated signaling pathway1.17e-05
IKBKBGO:0070423nucleotide-binding oligomerization domain containing signaling pathway1.33e-05
IKBKBGO:0035872nucleotide-binding domai3.20e-07
IKBKBGO:0045089positive regulation of innate immune response1.47e-05
IKBKBGO:0032607interferon-alpha production1.55e-05
IKBKBGO:0032647regulation of interferon-alpha production1.55e-05
IKBKBGO:0030522intracellular receptor signaling pathway1.64e-05
IKBKBGO:2001235positive regulation of apoptotic signaling pathway1.64e-05
IKBKBGO:0031098stress-activated protein kinase signaling cascade1.64e-05
IKBKBGO:0001819positive regulation of cytokine production1.84e-05
IKBKBGO:0051091positive regulation of DNA-binding transcription factor activity1.85e-05
IKBKBGO:0002237response to molecule of bacterial origin2.06e-05
IKBKBGO:0002833positive regulation of response to biotic stimulus2.06e-05
IKBKBGO:2000628regulation of miRNA metabolic process2.71e-05
IKBKBGO:0043433negative regulation of DNA-binding transcription factor activity3.26e-05
IKBKBGO:0001959regulation of cytokine-mediated signaling pathway3.67e-05
IKBKBGO:0060759regulation of response to cytokine stimulus5.34e-05

Top

Related Drugs to PER1_IKBKB


check button Drugs used for this fusion-positive patient.
(Manual curation of PubMed, 04-30-2022 + MyCancerGenome)
HgeneTgeneDrugSourcePMID

check button Distribution of the number of studies mentioning PER1-IKBKB and kinase inhibitors the PubMed Abstract (04-01-2024)

Fusion gene - drug pair 1Fusion gene - drug pair 2PMIDPublication dateDOIStudy title

Top

Related Diseases to PER1_IKBKB


check button Diseases that have this fusion gene.
(Manual curation of PubMed, 04-30-2022 + MyCancerGenome)
HgeneTgeneDiseaseSourcePMID

check button Related diseases from the literature mentioned this fusion gene and drug.
(PubMed, 04-01-2024)
MeSH IDMeSH term

check button Diseases associated with fusion partners.
(DisGeNet 4.0)
PartnerGeneDisease IDDisease name# pubmedsSource


Top

Clinical Trials of the Found Drugs/Small Molecules


check button Statistics of the Clinical Trials of the Found Kinase Inibitors from clinicaltrials.gov (06-17-2024)

check button Clinical Trials from clinicaltrials.gov (06-17-2024)

Fusion GeneKinase InhibitorNCT IDStudy StatusPhasesDisease# EnrolmentDate