| Name | Gap junction beta-1 protein | ||
| UniProt ID | CXB1_HUMAN | ||
| Gene Name | GJB1 | ||
| Gene ID | 2705 | ||
| Synonyms |
GJB1, CMTX, CMTX1, CX32
|
||
| Sequence |
MNWTGLYTLLSGVNRHSTAIGRVWLSVIFIFRIMVLVVAAESVWGDEKSSFICNTLQPGC
NSVCYDQFFPISHVRLWSLQLILVSTPALLVAMHVAHQQHIEKKMLRLEGHGDPLHLEEV KRHKVHISGTLWWTYVISVVFRLLFEAVFMYVFYLLYPGYAMVRLVKCDVYPCPNTVDCF VSRPTEKTVFTVFMLAASGICIILNVAEVVYLIIRACARRAQRRSNPPSRKGSGFGHRLS PEYKQNEINKLLSEQDGSLKDILRRSPGTGAGLAEKSDRCSAC |
||
| Pathway Map | MAP LINK | ||
| T.C. Number | 1.A.24.1.3 | ||
| KEGG ID | hsa2705 | ||
| TTD ID | T27984 | ||
| Pfam | PF00029 | ||
| Pair Name | Curcumin, HSV-TK/GCV | |||
| Phytochemical | Curcumin | |||
| Drug | HSV-TK/GCV | |||
| Disease Info | [ICD-11: 2C30] | Melanoma | Investigative | |
| Regulate Info | Up-regulation | Gap junction beta-1 protein | Expression | |
| Result | Curcumin could enhance the killing effect and the bystander effect of HSV-TK/GCV in treating melanoma, which might be mediated by improved gap junction. | |||
| Pair Name | Methylselenocysteine, Etoposide | |||
| Phytochemical | Methylselenocysteine | |||
| Drug | Etoposide | |||
| Disease Info | [ICD-11: 2C77] | Cervical cancer | Investigative | |
| Regulate Info | Up-regulation | Gap junction beta-1 protein | Expression | |
| Result | We provide the novel finding that MSC increases etoposide-mediated cytotoxicity by enhancing GJ activity, due to elevated Cx expression through a GSH-dependent posttranscriptional mechanism. More generally, the study highlights potential benefit of the combination of GJ modulators and chemotherapeutic agents in anticancer treatment. | |||
| No. | Title | Href |
|---|---|---|
| 1 | Curcumin plays a synergistic role in combination with HSV-TK/GCV in inhibiting growth of murine B16 melanoma cells and melanoma xenografts. PeerJ. 2019 Sep 20;7:e7760. doi: 10.7717/peerj.7760. | Click |
| 2 | Methylselenocysteine Potentiates Etoposide-Induced Cytotoxicity by Enhancing Gap Junction Activity. Biol Pharm Bull. 2022;45(4):467-476. doi: 10.1248/bpb.b21-00893. | Click |
