Molecule Information
General Information of the Molecule (ID: Mol04365)
| Name |
Tumor necrosis factor receptor superfamily member 3 (LTBR)
,Homo sapiens
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| Synonyms |
Lymphotoxin-beta receptor; Tumor necrosis factor C receptor; Tumor necrosis factor receptor 2-related protein; Tumor necrosis factor receptor type III
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| Molecule Type |
Protein
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| Gene Name |
LTBR
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| Gene ID | |||||
| Sequence |
MLLPWATSAPGLAWGPLVLGLFGLLAASQPQAVPPYASENQTCRDQEKEYYEPQHRICCS
RCPPGTYVSAKCSRIRDTVCATCAENSYNEHWNYLTICQLCRPCDPVMGLEEIAPCTSK R KTQCRCQPGMFCAAWALECTHCELLSDCPPGTEAELKDEVGKGNNHCVPCKAGHFQNT SS PSARCQPHTRCENQGLVEAAPGTAQSDTTCKNPLEPLPPEMSGTMLMLAVLLPLAFF LLL ATVFSCIWKSHPSLCRKLGSLLKRRPQGEGPNPVAGSWEPPKAHPYFPDLVQPLLP ISGD VSPVSTGLPAAPVLEAGVPQQQSPLDLTREPQLEPGEQSQVAHGTNGIHVTGGSM TITGN IYIYNGPVLGGPPGPGDLPATPEPPYPIPEEGDPGPPGLSTPHQEDGKAWHLAE TEHCGA TPSNRGPRNQFITHD Click to Show/Hide
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| Function |
Receptor for the heterotrimeric lymphotoxin containing LTAand LTB, and for TNFS14/LIGHT . Activates NF-kappa-Bsignaling pathway upon stimulation with lymphotoxin -LTB). Promotes apoptosis via TRAF3 and TRAF5. May play arole in the development of lymphoid organs.{ECO:0000269|PubMed:10799510, ECO:0000269|PubMed:24248355,ECO:0000269|PubMed:8171323}.
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Type(s) of Resistant Mechanism of This Molecule
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Multiple myeloma [ICD-11: 2A83.0] | [1] | |||
| Resistant Disease | Multiple myeloma [ICD-11: 2A83.0] | |||
| Resistant Drug | Bortezomib | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | NCI-H929 cells | Bone marrow | Homo sapiens (Human) | CVCL_1600 |
| Experiment for Molecule Alteration |
Western blot assay | |||
| Experiment for Drug Resistance |
MTT assay | |||
| Mechanism Description | In particular, the dynamic interaction between BM mesenchymal stem cells (BM-MSC) and MM cells has shown great relevance. Here we showed that inhibiting both PKC and NF-kappaB signalling pathways in BM-MSC reduced cell survival in the MM cell line H929 and increased its susceptibility to the proteasome inhibitor bortezomib. PKC-mediated cell survival inhibition and bortezomib susceptibility induction were better performed by the chimeric peptide HKPS than by the classical enzastaurin inhibitor, probably due to its greatest ability to inhibit cell adhesion and its increased capability to counteract the NF-kappaB-related signalling molecules increased by the co-cultivation of BM-MSC with H929 cells. Thus, inhibiting two coupled signalling molecules in BM-MSC was more effective in blocking the supportive cues emerging from the mesenchymal stroma. | |||
References
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