General Information of the Molecule (ID: Mol04314)
Name
DNA nucleotidylexotransferase (DNTT) ,Homo sapiens
Synonyms
Terminal addition enzyme; Terminal deoxynucleotidyltransferase
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Molecule Type
Protein
Gene Name
DNTT
Gene ID
1791
Sequence
MDPPRASHLSPRKKRPRQTGALMASSPQDIKFQDLVVFILEKKMGTTRRAFLMELARRKG
FRVENELSDSVTHIVAENNSGSDVLEWLQAQKVQVSSQPELLDVSWLIECIRAGKPVEM
T GKHQLVVRRDYSDSTNPGPPKTPPIAVQKISQYACQRRTTLNNCNQIFTDAFDILAEN
CE FRENEDSCVTFMRAASVLKSLPFTIISMKDTEGIPCLGSKVKGIIEEIIEDGESSEV
KAV LNDERYQSFKLFTSVFGVGLKTSEKWFRMGFRTLSKVRSDKSLKFTRMQKAGFLYY
EDLV SCVTRAEAEAVSVLVKEAVWAFLPDAFVTMTGGFRRGKKMGHDVDFLITSPGSTE
DEEQL LQKVMNLWEKKGLLLYYDLVESTFEKLRLPSRKVDALDHFQKCFLIFKLPRQRV
DSDQSS WQEGKTWKAIRVDLVLCPYERRAFALLGWTGSRQFERDLRRYATHERKMILDN
HALYDKT KRIFLKAESEEEIFAHLGLDYIEPWERNA
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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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Uniprot ID
TDT_HUMAN
Ensembl ID
ENSG000001074478
HGNC ID
HGNC:2983
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Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens
Type(s) of Resistant Mechanism of This Molecule
  ADTT: Aberration of the Drug's Therapeutic Target
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
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Inotuzumab ozogamicin
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
  Aberration of the Drug's Therapeutic Target (ADTT) Click to Show/Hide
Disease Class: Mature B-cell neoplasms [.] [1]
Resistant Disease Mature B-cell neoplasms [.]
Resistant Drug Inotuzumab ozogamicin
Molecule Alteration Missense mutation
p.R183W
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
Ref 1 Genomic determinants of response and resistance to inotuzumab ozogamicin in B-cell ALL. Blood. 2024 Jul 4;144(1):61-73.

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