Allosteric inhibition of HTRA1 activity by a conformational lock mechanism to treat age-related macular degeneration.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
05 09 2022
Historique:
received: 03 02 2022
accepted: 16 08 2022
entrez: 6 9 2022
pubmed: 7 9 2022
medline: 9 9 2022
Statut: epublish

Résumé

The trimeric serine protease HTRA1 is a genetic risk factor associated with geographic atrophy (GA), a currently untreatable form of age-related macular degeneration. Here, we describe the allosteric inhibition mechanism of HTRA1 by a clinical Fab fragment, currently being evaluated for GA treatment. Using cryo-EM, X-ray crystallography and biochemical assays we identify the exposed LoopA of HTRA1 as the sole Fab epitope, which is approximately 30 Å away from the active site. The cryo-EM structure of the HTRA1:Fab complex in combination with molecular dynamics simulations revealed that Fab binding to LoopA locks HTRA1 in a non-competent conformational state, incapable of supporting catalysis. Moreover, grafting the HTRA1-LoopA epitope onto HTRA2 and HTRA3 transferred the allosteric inhibition mechanism. This suggests a conserved conformational lock mechanism across the HTRA family and a critical role of LoopA for catalysis, which was supported by the reduced activity of HTRA1-3 upon LoopA deletion or perturbation. This study reveals the long-range inhibition mechanism of the clinical Fab and identifies an essential function of the exposed LoopA for activity of HTRA family proteases.

Identifiants

pubmed: 36064790
doi: 10.1038/s41467-022-32760-9
pii: 10.1038/s41467-022-32760-9
pmc: PMC9445180
doi:

Substances chimiques

Epitopes 0
Immunoglobulin Fab Fragments 0
HTRA3 protein, human EC 3.4.21.-
High-Temperature Requirement A Serine Peptidase 1 EC 3.4.21.-
HTRA1 protein, human EC 3.4.21.-
Serine Endopeptidases EC 3.4.21.-

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

5222

Subventions

Organisme : NIGMS NIH HHS
ID : P30 GM133894
Pays : United States

Informations de copyright

© 2022. The Author(s).

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Auteurs

Stefan Gerhardy (S)

Department of Early Discovery Biochemistry, Genentech Inc., San Francisco, CA, USA.

Mark Ultsch (M)

Department of Structural Biology, Genentech Inc., San Francisco, CA, USA.

Wanjian Tang (W)

Department of Early Discovery Biochemistry, Genentech Inc., San Francisco, CA, USA.

Evan Green (E)

Department of Structural Biology, Genentech Inc., San Francisco, CA, USA.

Jeffrey K Holden (JK)

Department of Early Discovery Biochemistry, Genentech Inc., San Francisco, CA, USA.

Wei Li (W)

Department of Early Discovery Biochemistry, Genentech Inc., San Francisco, CA, USA.

Alberto Estevez (A)

Department of Structural Biology, Genentech Inc., San Francisco, CA, USA.

Chris Arthur (C)

Department of Structural Biology, Genentech Inc., San Francisco, CA, USA.

Irene Tom (I)

Department of OMNI Biomarker Development, Genentech Inc., San Francisco, CA, USA.

Alexis Rohou (A)

Department of Structural Biology, Genentech Inc., San Francisco, CA, USA.

Daniel Kirchhofer (D)

Department of Early Discovery Biochemistry, Genentech Inc., San Francisco, CA, USA. dak@gene.com.

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