Target intelligence / Profile preview

CMT1A duplicated region transcript 15 protein (CDRT15)

Target
CDRT15
Molecular classification
Other (not assigned to any common target class such as receptor, enzyme, ion channel, transporter, or transcription factor)
01

Overview

CMT1A duplicated region transcript 15 protein (CDRT15) is a protein-coding gene located within the 1.4 Mb CMT1A duplication region of chromosome 17, which is implicated in the pathogenesis of Charcot–Marie–Tooth disease type 1A and hereditary neuropathy with liability to pressure palsy[1][4][6][7]. The biological function of CDRT15 is poorly characterized; it is a gene discovered during genomic mapping of this disease locus and may represent a recently evolved or primate-specific genetic element[4]. Unlike PMP22, which is directly implicated in disease pathogenesis through copy number variation, CDRT15 is not known to be a therapeutic target, nor does it serve as a biomarker or have established disease relevance beyond its genomic proximity to the CMT1A region. No drugs are known to interact with CDRT15, and no mechanism of action is described for targeting this protein. Existing literature and genomic databases do not assign it to a traditional molecular target class (e.g., "receptor," "enzyme") or ascribe it confirmed biological function or therapeutic relevance[4][7].

Other names
CMT1A duplicated region transcript 15CDRT15CDRT15 proteinCDRTF_HUMAN (UniProt)NCBI Gene: 146822HGNC:14395Ensembl: ENSG00000223510
02

Mechanism of action

Not applicable; no drugs target CDRT15.

03

Biological functions

Unknown The precise biological function of CDRT15 is not established; it is identified in a genomic region with complex structural variation and may be expressed during embryogenesis or development[4].
04

Disease associations

Hereditary neuropathy, with liability to pressure palsyPossibly implicated in Charcot–Marie–Tooth disease type 1A (as a gene present in the pathogenic duplication region, but not the causative gene, which is PMP22)[4][7]Role in disease is speculative and not well supported as a direct causal factor

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