Target intelligence / Profile preview

Transmembrane protein 161B (TMEM161B)

Target
TMEM161B
Molecular classification
Other (multi-pass transmembrane protein; not classified as a receptor, enzyme, transporter, ion channel, or transcription factor)
01

Overview

Transmembrane protein 161B (TMEM161B) is an evolutionarily conserved, widely expressed, multi-pass transmembrane protein with 8–9 predicted transmembrane segments. It is not homologous to established protein families such as receptors, channels, enzymes, or transporters, and lacks annotated functional domains. TMEM161B plays an essential role in mammalian brain development, especially in regulating the organization and polarity of neural progenitor cells and modulating the cytoskeleton via actin filopodia. Loss-of-function mutations in TMEM161B cause severe developmental brain disorders in humans, particularly polymicrogyria, intellectual disability, and epilepsy, and similar neurodevelopmental phenotypes in animal models. TMEM161B is also required for the structure and function of primary cilia in neural tissues and mediates Sonic Hedgehog signaling during central nervous system patterning. Current data do not establish TMEM161B as a direct therapeutic target or receptor, nor are there any approved drugs known to directly interact with it.

Other names
TMEM161BUNQ679/PRO1313MGC33214FLB3342PRO1313
02

Biological functions

Regulation of actin cytoskeleton dynamicsModulation of radial glial scaffolding and apical-basal polarity in neural precursorsRegulation of primary cilium structure and function, particularly in neural tissueRegulation of Sonic Hedgehog (Shh) signalingRegulation of cerebral cortical gyration (folding) and brain developmentControl of action potential dynamics in excitable cells (cardiomyocytes in some species)
03

Disease associations

Polymicrogyria (PMG; malformation of cortical development)Intellectual disabilityEpilepsy/seizures (related to PMG)Holoprosencephaly (severe neural tube and brain patterning defect in null mice)Cardiac rhythm disturbance (in model organisms)
04

Safety considerations

No data; knockout or deleterious variants lead to severe brain developmental disorders and, in animal models, to lethal neural defects

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