TEX264: Testis-Expressed Protein 264
A key regulator of ER-phagy and selective autophagy, implicated in cellular stress responses and cancer.
Gene Information Card
| Symbol | TEX264 |
|---|---|
| Full Name | Testis-Expressed Protein 264 |
| Gene Type | Protein coding |
| Chromosomal Location | 3p21.31 |
| NCBI Gene ID | 113174 ncbi.nlm.nih.gov/gene/113174 |
| Ensembl ID | ENSG00000164078 |
| UniProt ID | Q9Y6I9 |
| OMIM ID | 617956 |
| HGNC ID | 29242 |
| Aliases | FLJ11273, ZSIG11 |
Description
TEX264 (Testis-Expressed Protein 264) encodes a single-pass transmembrane protein that functions as a selective autophagy receptor for endoplasmic reticulum (ER) turnover (ER-phagy). It is widely expressed, with highest levels in testis, and plays a critical role in maintaining ER homeostasis by targeting damaged or excess ER fragments to lysosomes. TEX264 is also involved in cellular stress responses and has been implicated in cancer biology through its regulation of autophagy.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Cancer (various) | TEX264 mutations may alter ER-phagy, affecting tumor cell survival under stress. | COSMIC; somatic mutations found in multiple cancer types. |
| Neurodegenerative disorders (potential) | Impaired ER-phagy due to TEX264 dysfunction could contribute to protein aggregation. | Inferred from autophagy pathway; no direct ClinVar entries. |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Testis | 45.2 | High |
| Thyroid | 18.7 | Medium |
| Adrenal gland | 15.3 | Medium |
| Brain | 8.1 | Low |
| Liver | 6.4 | Low |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| HEK 293 | 22.5 | Embryonic kidney; model for autophagy studies |
| HeLa | 18.9 | Cervical cancer; high expression |
| K562 | 12.3 | Leukemia; moderate expression |
| HepG2 | 9.8 | Liver cancer; low expression |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.487C>T (p.Arg163Trp) | Missense | 0.02% (gnomAD) | Unknown; may affect protein stability |
| c.632_633del (p.Leu211ProfsTer12) | Frameshift | Rare | Predicted loss of function; truncation of C-terminal domain |
Mutation functional classification
Loss of Function (LOF)
Frameshift mutations (e.g., p.Leu211ProfsTer12) are predicted to cause loss of function by truncating the protein, impairing ER-phagy receptor activity.
Gain of Function (GOF)
No documented gain-of-function mutations for TEX264.
Dominant Negative (DN)
No evidence of dominant-negative effects for TEX264 mutations.
View complete mutation data：
Gene Ontology (GO)
| • autophagosome (GO:0005776) | • endoplasmic reticulum (GO:0005783) |
| • macroautophagy (GO:0016236) | • positive regulation of protein binding (GO:0032092) |
| • identical protein binding (GO:0042802) |
Pathways
• Selective autophagy (ER-phagy)
• Endoplasmic reticulum stress response
Protein Summary
TEX264 is a 264-amino acid single-pass transmembrane protein localized to the endoplasmic reticulum. It acts as an ER-phagy receptor, binding to LC3/GABARAP family proteins via its LIR motif to mediate autophagic degradation of ER fragments. The protein contains a conserved C-terminal domain essential for receptor function. TEX264 is ubiquitously expressed but enriched in testis, and its dysregulation is linked to cancer and cellular stress.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| TEX264 Knockout HEK293 Cell Line | EDJ-KQ11072 | Human | 51368 | Details Get a Quote |
| TEX264 Knockout A-549 Cell Line | EDJ-KQ38993 | Human | 51368 | Details Get a Quote |
| TEX264 Knockout HCT 116 Cell Line | EDJ-KQ38994 | Human | 51368 | Details Get a Quote |
| TEX264 Knockout HeLa Cell Line | EDJ-KQ38995 | Human | 51368 | Details Get a Quote |
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