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Transmembrane 9 superfamily member 1 (TM9SF1)

Target: TM9SF1
Molecular classification: Other (nonaspanin family; transmembrane protein with nine transmembrane domains; not a classical receptor, ion channel, enzyme, or transporter)

Overview

Transmembrane 9 superfamily member 1 (TM9SF1) is a widely expressed, evolutionarily conserved multispanning membrane protein, distinguished by its nine transmembrane domains and large non-cytoplasmic N-terminal region[1][2]. TM9SF1 belongs to the nonaspanin family, with no known classical receptor, transporter, or enzyme activity. Its functional characterization is still emerging: it promotes the autophagic degradation of Vimentin and acts as a tumor metastasis suppressor in colorectal cancer by reducing cell migration and invasion through regulation of filopodium-like protrusions[1]. TM9SF1 regulates autophagy in a context-dependent manner and is implicated in inflammatory processes, notably acute lung injury, where it may act as a negative regulator of autophagy and drive inflammatory damage[2]. Currently, there are no drugs known to directly target TM9SF1, and it is not considered a validated therapeutic target. More research is needed to elucidate its molecular interactions and potential for therapeutic intervention.

Other names: TM9SF1hMP70MP70HMP70MP70 protein family membermultispanning membrane protein (70kD)transmembrane protein 9 superfamily member 1

Biological functions

Autophagy regulation (context-dependent: can promote or suppress autophagy depending on cell type)Cytoskeleton regulation (interacts with Vimentin, regulates cell motility and structural dynamics)Modulation of cancer metastasis (suppresses colorectal cancer cell migration and metastasis)Modulation of inflammatory response (involved in acute lung injury models)

Disease associations

Cancer (acts as tumor metastasis suppressor in colorectal cancer; promotes cell motility in bladder cancer; context-dependent roles)Inflammation (upregulated in acute lung injury, promotes injury progression via autophagy regulation)

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