9.B.208.1.2 The bile acid farnesoid receptor, FXR, of 472 or 486 aas but 0 TMSs. The farnesoid X receptor is an important target for the treatment of disorders of bile acid and fatty acid metabolism in mice with nonalcoholic fatty liver disease combined with cholestasis (Liu et al. 2023). FXR, MRP-1 and SLC7A5 are new targets for the treatment of hepatocellular carcinoma (Zhang et al. 2024). SLC7A11, a key protein involved in ferroptosis, and it has been identified as a
potential target for drug development. Through screening efforts, novel
inhibitors of SLC7A11 have been designed with the aim of promoting
ferroptosis and ultimately eliminating cancer cells. Small molecules 42711 and 27363 have been identified as lead compounds with strong inhibitory
activity against SLC7A11. Further optimization resulted in the
development of a new inhibitor structure (42711_11) (Zhang et al. 2024). FXR-deficiency induces ferroptosis via modulation
of CBP-dependent p53 acetylation to suppress breast cancer growth
and metastasis (Huang et al. 2024). FXR was first reported as a tumor promoter that enhanced the
proliferation and metastasis of breast cancer cells by regulating
CBP-dependent p53 K382 acetylation. FXR may serve as a therapeutic target for the treatment of breast cancer.
|
Accession Number: | B6ZGS9 |
Protein Name: | Farnesoid X receptor |
Length: | 472 |
Molecular Weight: | 54409.00 |
Species: | Homo sapiens (Human) [9606] |
Location1 / Topology2 / Orientation3: |
Nucleus1 |
Substrate |
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1: MGSKMNLIEH SHLPTTDEFS FSENLFGVLT EQVAGPLGQN LEVEPYSQYS NVQFPQVQPQ
61: ISSSSYYSNL GFYPQQPEEW YSPGIYELRR MPAETLYQGE TEVAEMPVTK KPRMGASAGR
121: IKGDELCVVC GDRASGYHYN ALTCEGCKGF FRRSITKNAV YKCKNGGNCV MDMYMRRKCQ
181: ECRLRKCKEM GMLAECLLTE IQCKSKRLRK NVKQHADQTV NEDSEGRDLR QVTSTTKSCR
241: EKTELTPDQQ TLLHFIMDSY NKQRMPQEIT NKILKEEFSA EENFLILTEM ATNHVQVLVE
301: FTKKLPGFQT LDHEDQIALL KGSAVEAMFL RSAEIFNKKL PSGHSDLLEE RIRNSGISDE
361: YITPMFSFYK SIGELKMTQE EYALLTAIVI LSPDRQYIKD REAVEKLQEP LLDVLQKLCK
421: IHQPENPQHF ACLLGRLTEL RTFNHHHAEM LMSWRVNDHK FTPLLCEIWD VQ