Phagophore assembly factor 1 (PHAF1)

Phagophore assembly factor 1 (PHAF1; also known as MYTHO, C16orf6, or C16orf70) is an evolutionarily conserved protein that plays a critical regulatory role in the initiation of macroautophagy, a key cellular degradation and recycling pathway[1][2][4]. PHAF1 acts as a molecular scaffold at the phagophore assembly site (PAS), facilitating the recruitment and assembly of autophagy machinery components like WIPI2 and BCAS3, leading to autophagosome formation[1][4]. PHAF1 is transcriptionally regulated (including by the FoxO pathway) and upregulated in response to multiple catabolic and aging contexts[2]. Experimental knockdown or deletion of PHAF1 impairs autophagic flux, results in muscle atrophy resistance during acute stress but induces severe myopathic changes if suppressed long-term, including inflammation, abnormal calcium handling, and myofiber degeneration[2]. Overexpression leads to muscle wasting. PHAF1 is not currently recognized as a direct therapeutic target — there are no known drugs or interventions directly modulating this protein — but it has disease relevance in conditions of altered muscle autophagy or aging[4][2][1]. Note: - PHAF1 is not a receptor, enzyme, or classical drug target but rather a scaffold protein essential for autophagy, muscle integrity, and organismal aging[1][2][4]. - No direct pharmacological modulators or clinical biomarkers for PHAF1 are currently established[1][4]. - Aliases and previous symbols are well-documented (see above), but confusion may arise due to multiple alternative names and historical gene identifiers[1][4]. - Is_incorrect: true, because this molecule is not a confirmed therapeutic target (e.g., receptor, enzyme, transporter) and some aliases (e.g., lin-10, C16orf70) could refer to other gene contexts.

Other names

MYTHOC16orf6C16orf70lin-10FLJ12076macro-autophagy and youth optimizerLIN10UPF0183 protein C16orf70

Not applicable (no known pharmacological modulators reported in the literature)