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Protein O-mannosyl-transferase TMTC4 (TMTC4)
- Target
- TMTC4
- Molecular classification
- Enzyme (O-mannosyltransferase), Transmembrane protein (contains 10 transmembrane regions), Tetratricopeptide repeat (TPR) protein family member
01
Overview
Protein O-mannosyl-transferase TMTC4 is a transmembrane, ER-localized glycosyltransferase belonging to the TMTC protein family. It contains 10 transmembrane domains and multiple tetratricopeptide repeats in its C-terminal region. TMTC4 catalyzes the addition of mannose residues to serine or threonine hydroxyl groups, primarily targeting cadherin-like domains. TMTC4 is expressed in all human tissues, with highest levels in the brain and spinal cord. Functional disruption of TMTC4 can impair cell adhesion, induce hearing loss, and contribute to bone density abnormalities. TMTC4 is implicated in the regulation of the unfolded protein response, ER stress, and may play roles in neurological, immune, and metabolic disease mechanisms. TMTC4 interacts with cadherins, PDIA3, and other proteins involved in cell adhesion and protein folding[1][2][3][4][5].
- Other names
- TMTC4Transmembrane O-mannosyltransferase targeting cadherins 4Transmembrane and tetratricopeptide repeat-containing 4FLJ14624FLJ22153DFNB122Protein O-mannosyl-transferase TMTC4Transmembrane and TPR repeat-containing protein 4Transmembrane and tetratricopeptide repeat containing 4
02
Mechanism of action
Inhibition or modulation of TMTC4’s O-mannosyltransferase activity, potentially affecting O-mannosylation of cadherins and cell adhesion processes.
03
Biological functions
O-mannosylation of cadherin domains (transfers mannose to serine/threonine hydroxyl groups)Endoplasmic reticulum stress response and unfolded protein responseCellular stress responsesBone density regulation (suggested)Potential involvement in synaptic vesicle fusion, protein folding, and protein translocation (via TPR domain interactions)
04
Disease associations
Deafness, Autosomal Recessive 122 (rapid postnatal death of cochlear hair cells in mouse models)Bone density disorders (suggested by association studies)Suprabulbar paresis (congenital)Potential implications in neurological, immune, and metabolic disorders
05
Safety considerations
Loss of TMTC4 function may cause hearing loss and bone density defects in mouse modelsTargeting TMTC4 could affect the ER stress response and protein glycosylation, with potential implications for cell adhesion and organ development
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