RNFT1

Details:

UniProt Entry: Q5M7Z0
Gene: RNFT1
Class: RING
Family: RING4
Protein length: 435
Database confidence: 0.75
InterPro: InterPro Entry
Mode of Action: Standalone
AlphaFold Model: Link

Protein Sequence ▾

>Q5M7Z0
MPLFLLSLPT PPSASGHERR QRPEAKTSGS EKKYLRAMQA NRSQLHSPPG TGSSEDASTP
QCVHTRLTGE GSCPHSGDVH IQINSIPKEC AENASSRNIR SGVHSCAHGC VHSRLRGHSH
SEARLTDDTA AESGDHGSSS FSEFRYLFKW LQKSLPYILI LSVKLVMQHI TGISLGIGLL
TTFMYANKSI VNQVFLRERS SKIQCAWLLV FLAGSSVLLY YTFHSQSLYY SLIFLNPTLD
HLSFWEVFWI VGITDFILKF FFMGLKCLIL LVPSFIMPFK SKGYWYMLLE ELCQYYRTFV
PIPVWFRYLI SYGEFGNVTR WSLGILLALL YLILKLLEFF GHLRTFRQVL RIFFTQPSYG
VAASKRQCSD VDDICSICQA EFQKPILLIC QHIFCEECMT LWFNREKTCP LCRTVISDHI
NKWKDGATSS HLQIY

Domain Architecture (From InterPro) ▾

Start	End	Type	Name	InterPro	Source
43	435	Family	RING finger and transmembrane domain-containing protein 1/2	IPR044235	PTHR15860
360	433	Homologous_superfamily	Zinc finger, RING/FYVE/PHD-type	IPR013083	G3DSA:3.30.40.10
375	413	Domain	Zinc finger, RING-type	IPR001841	PS50089
375	412	Domain	Zinc finger, RING-type	IPR001841	SM00184
390	399	Conserved_site	Zinc finger, RING-type, conserved site	IPR017907	PS00518

Protein functions ▾

GO term	Name	Ontology	Evidence	Reference
GO:1904294	positive regulation of ERAD pathway	Biological Process	IEA	GO_REF:0000002
GO:0016567	protein ubiquitination	Biological Process	IEA	GO_REF:0000041
GO:0051865	protein autoubiquitination	Biological Process	IDA	PMID:27485036
GO:0016020	membrane	Cellular Component	IEA	GO_REF:0000043
GO:0012505	endomembrane system	Cellular Component	IEA	GO_REF:0000044
GO:0005783	endoplasmic reticulum	Cellular Component	IBA	GO_REF:0000033
GO:0005789	endoplasmic reticulum membrane	Cellular Component	IEA	GO_REF:0000044
GO:0016740	transferase activity	Molecular Function	IEA	GO_REF:0000043
GO:0061630	ubiquitin protein ligase activity	Molecular Function	IEA	GO_REF:0000002
GO:0008270	zinc ion binding	Molecular Function	IEA	GO_REF:0000043
GO:0043130	ubiquitin binding	Molecular Function	IDA	PMID:27485036
GO:0046872	metal ion binding	Molecular Function	IEA	GO_REF:0000043

Enzyme–Substrate Interactions ▾

Data Usage Statement and License Agreement

Ownership and Copyright

The Database, including all associated datasets, metadata, and documentation, is the intellectual property of the PROXIDRUGs consortium and the InnoDATA project.
The content of the Database is protected under applicable copyright and database protection laws.

Permitted Use

The Database is provided for research, academic, and non-commercial purposes only, unless explicitly stated otherwise.
Users are permitted to:
- Access, download, and use the data.
- Modify or build upon the data for academic, educational, or scientific purposes.
- Share derived datasets, analyses, or visualizations with proper citation and explicit acknowledgment of “The Human E3 Ligome” project.

Prohibited Use

Use the Database or any derivative works for commercial purposes without prior written consent from the PROXIDRUGs consortia (InnoDATA PIs).
Redistribute or republish the Database (or substantial parts of it) without proper credit and adherence to the license terms.
Misrepresent the data, alter metadata to mislead, or use it in a way that violates ethical or scientific standards.

Licensing

Unless otherwise stated, the Database is licensed under the Creative Commons Attribution 4.0 International License (CC BY 4.0).
This license allows redistribution and adaptation, provided appropriate credit is given.
Contributions (e.g., data corrections, additions, or scripts) can be made through merge requests on GitLab.
Contributors must agree to license their contributions under the same CC BY 4.0 license.

Citation Requirements

If you use or refer to the Database in your publications, reports, or presentations, you must cite the paper: Dutta et al. (2025, preprint)

Contact and Support

For inquiries, permissions, or support regarding the Database, please contact: Dr. Ramachandra M. Bhaskara, Goethe University Frankfurt.
Email: bhaskara@med.uni-frankfurt.de.
Website maintained by Alberto Cristiani, Arghya Dutta, and Siddhanta V. Nikte.