JTB jumping translocation breakpoint [Homo sapiens (human)] - Gene

Summary

Official Symbol: JTBprovided by HGNC
Official Full Name: jumping translocation breakpointprovided by HGNC
Primary source: HGNC:HGNC:6201
See related: Ensembl:ENSG00000143543 MIM:604671; AllianceGenome:HGNC:6201
Gene type: protein coding
RefSeq status: VALIDATED
Organism: Homo sapiens
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo
Also known as: PAR; hJT; HJTB; HSPC222
Summary: Enables protein kinase binding activity. Involved in mitotic cytokinesis and positive regulation of protein kinase activity. Located in cytoplasm; microtubule cytoskeleton; and midbody. [provided by Alliance of Genome Resources, Nov 2024]
Expression: Ubiquitous expression in colon (RPKM 43.4), stomach (RPKM 38.7) and 25 other tissues See more
Orthologs: mouse all
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Genomic context

Location:: 1q21.3

Exon count:: 5

Annotation release	Status	Assembly	Chr	Location
RS_2024_08	current	GRCh38.p14 (GCF_000001405.40)	1	NC_000001.11 (153974269..153977674, complement)
RS_2024_08	current	T2T-CHM13v2.0 (GCF_009914755.1)	1	NC_060925.1 (153111532..153114937, complement)
RS_2024_09	previous assembly	GRCh37.p13 (GCF_000001405.25)	1	NC_000001.10 (153946745..153950150, complement)

Chromosome 1 - NC_000001.11 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

Go to nucleotide: Graphics FASTA GenBank

Expression

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See details

Project title: HPA RNA-seq normal tissues HPA RNA-seq normal tissues
Description: RNA-seq was performed of tissue samples from 95 human individuals representing 27 different tissues in order to determine tissue-specificity of all protein-coding genes
BioProject: PRJEB4337
Publication: PMID 24309898
Analysis date: Wed Apr 4 07:08:55 2018

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

Downregulation of the PAR expression increases the Bax/Bcl-2 ratio and Bax expression, and thus induces the G2-M phase arrest and apoptosis of PC3 cells.
Title: [Downregulation of PAR expression induces the apoptosis of human prostate cancer PC3 cells and increases the Bcl-2/Bax ratio].
The JTB structure has a distant relationship to the midkine/pleiotrophin fold, particularly in the conservation of distinctive disulfide bridge patterns.
Title: The structure of the extracellular domain of the jumping translocation breakpoint protein reveals a variation of the midkine fold.
Due to its involvement in cell cycle and its overexpression in several human cancers PAR could represent an attractive target for therapeutic intervention.
Title: PAR, a protein involved in the cell cycle, is functionally related to chromosomal passenger proteins.
Overexpression of JTB conferred resistance to apoptosis induced by ultraviolet radiation
Title: Interacting with HBsAg compromises resistance of jumping translocation breakpoint protein to ultraviolet radiation-induced apoptosis in 293FT cells.
Among ten hepatocellular carcinoma cases with amplicon 1q21-q22, significant gene expression level of JTB, SHC1, CCT3 and COPA in the tumors than the paired adjacent non-malignant liver tissues.
Title: Positional mapping for amplified DNA sequences on 1q21-q22 in hepatocellular carcinoma indicates candidate genes over-expression.

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Phenotypes

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Find tests for this gene in the NIH Genetic Testing Registry (GTR)

Review eQTL and phenotype association data in this region using PheGenI

Variation

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See variants in ClinVar

See studies and variants in dbVar

See Variation Viewer (GRCh37.p13)

See Variation Viewer (GRCh38)

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Markers

RH63845 (e-PCR)
- UniSTS:41500

RH11825 (e-PCR)
- UniSTS:56352

A004O27 (e-PCR)
- UniSTS:7039

RH67852 (e-PCR)
- UniSTS:91332

Gene Ontology Provided by GOA

Function	Evidence Code	Pubs
enables protein kinase binding	IDA Inferred from Direct Assay more info	PubMed

Process	Evidence Code	Pubs
involved_in apoptotic mitochondrial changes	IEA Inferred from Electronic Annotation more info
involved_in mitotic cell cycle	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in mitotic cytokinesis	IBA Inferred from Biological aspect of Ancestor more info
involved_in mitotic cytokinesis	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in positive regulation of protein kinase activity	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in regulation of cell population proliferation	IEA Inferred from Electronic Annotation more info

Component	Evidence Code	Pubs
colocalizes_with centrosome	IBA Inferred from Biological aspect of Ancestor more info
colocalizes_with centrosome	IDA Inferred from Direct Assay more info	PubMed
is_active_in cytoplasm	IBA Inferred from Biological aspect of Ancestor more info
located_in cytoplasm	IDA Inferred from Direct Assay more info	PubMed
located_in membrane	TAS Traceable Author Statement more info	PubMed
is_active_in midbody	IBA Inferred from Biological aspect of Ancestor more info
located_in midbody	IDA Inferred from Direct Assay more info	PubMed
located_in mitochondrion	IEA Inferred from Electronic Annotation more info
located_in plasma membrane	TAS Traceable Author Statement more info	PubMed
colocalizes_with spindle	IBA Inferred from Biological aspect of Ancestor more info
colocalizes_with spindle	IDA Inferred from Direct Assay more info	PubMed

General protein information

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Preferred Names: protein JTB

Names: jumping translocation breakpoint protein; prostate androgen-regulated protein

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.