Molecule Information
General Information of the Molecule (ID: Mol04314)
| Name |
DNA nucleotidylexotransferase (DNTT)
,Homo sapiens
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| Synonyms |
Terminal addition enzyme; Terminal deoxynucleotidyltransferase
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| Molecule Type |
Protein
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| Gene Name |
DNTT
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| Gene ID | |||||
| Sequence |
MDPPRASHLSPRKKRPRQTGALMASSPQDIKFQDLVVFILEKKMGTTRRAFLMELARRKG
FRVENELSDSVTHIVAENNSGSDVLEWLQAQKVQVSSQPELLDVSWLIECIRAGKPVEM T GKHQLVVRRDYSDSTNPGPPKTPPIAVQKISQYACQRRTTLNNCNQIFTDAFDILAEN CE FRENEDSCVTFMRAASVLKSLPFTIISMKDTEGIPCLGSKVKGIIEEIIEDGESSEV KAV LNDERYQSFKLFTSVFGVGLKTSEKWFRMGFRTLSKVRSDKSLKFTRMQKAGFLYY EDLV SCVTRAEAEAVSVLVKEAVWAFLPDAFVTMTGGFRRGKKMGHDVDFLITSPGSTE DEEQL LQKVMNLWEKKGLLLYYDLVESTFEKLRLPSRKVDALDHFQKCFLIFKLPRQRV DSDQSS WQEGKTWKAIRVDLVLCPYERRAFALLGWTGSRQFERDLRRYATHERKMILDN HALYDKT KRIFLKAESEEEIFAHLGLDYIEPWERNA Click to Show/Hide
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| Function |
Template-independent DNA polymerase which catalyzes therandom addition of deoxynucleoside 5'-triphosphate to the 3'-end of aDNA initiator. One of the in vivo functions of this enzyme is theaddition of nucleotides at the junction of rearranged Igheavy chain and T-cell receptor gene segments during the maturation ofB- and T-cells. {ECO:0000250|UniProtKB:P09838}.
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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: Mature B-cell neoplasms [.] | [1] | |||
| Resistant Disease | Mature B-cell neoplasms [.] | |||
| Resistant Drug | Inotuzumab ozogamicin | |||
| Molecule Alteration | Missense mutation | p.R183W |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | pre-InO and/or post-InO tumor cells | N.A. | Homo sapiens (Human) | N.A. |
| Experiment for Molecule Alteration |
GeneSeq assay; Mutation assay | |||
| Mechanism Description | Multiple mechanisms drive CD22 antigen escape, including epitope loss (protein truncation and destabilization) and epitope alteration.Hypermutation caused by error-prone DNA damage repair may serve as a driver of CD22 mutation and escape. | |||
References
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