Target intelligence / Profile preview

HAUS augmin-like complex subunit 3 (HAUS3)

Target
HAUS3
Molecular classification
Other (Component of multi-protein complex, specifically augmin complex), Not a receptor, enzyme, transporter, ion channel, transcription factor, or histone modification protein
01

Overview

HAUS augmin-like complex subunit 3 (HAUS3) is a structural protein encoded by the HAUS3 gene and is a key component of the augmin complex, a hetero-octameric assembly required for robust microtubule nucleation within the mitotic spindle during cell division[2][4]. HAUS3 forms a dimer with HAUS5, contributing to the architecture and stability of the TIII tetramer subunit of the augmin complex[3][1][7]. The augmin complex, including HAUS3, is responsible for recruiting γ-tubulin to spindle microtubules, which is crucial for their organization, chromosome segregation, and integrity of centrosomes[2][4][1]. Loss or dysfunction of HAUS3 causes mitotic defects such as spindle disorder and fragmentation of centrosomes, which can contribute to carcinogenesis and other proliferative disorders[2][4]. HAUS3 is not classified as a receptor, enzyme, ion channel, or transporter, but rather as a structural element of a multi-protein complex critical for cell division. No direct therapeutic drugs or biomarkers are associated with HAUS3 to date[2][4].

Other names
IT1DGT3C4orf15MGC4701
02

Mechanism of action

Not applicable. No drugs are known to directly target HAUS3. Mechanistic modulation would involve disruption of spindle assembly, but this is not clinically pursued.

03

Biological functions

Mitotic spindle assemblyCentrosome integrityMicrotubule nucleation and organizationCompletion of cytokinesis
04

Disease associations

Cancer (defects in augmin complex members contribute to mitotic errors, centrosome fragmentation, and cell division defects associated with carcinogenesis)Other (potential involvement in diseases of cell division, but not well-documented directly for HAUS3)
05

Safety considerations

None specific to HAUS3. Disruption of the augmin complex can cause mitotic defects, but there are no approved therapies or targeted safety concerns linked to HAUS3 modulation

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