General Information of the Molecule (ID: Mol02027)
Name
Ribosomal tetracycline resistance protein tet (TET(44)) ,Clostridioides difficile
Synonyms
BGV00_19340; BN1095_620053; BN1096_520088; BN1097_680096; E5F26_13010; E5F27_11275; E5F28_08645; E5F29_03080; E5F30_14860; E5F31_09375; E5F32_08895; E5F33_19320; E5F34_11670; E5F35_02795; E5F36_15070; E5F37_19425; E5F38_19050; E5F39_10665; E5F40_01415; E5F41_11825; E5F42_18275; E5F43_02490; E5F44_06595; E5F45_10465
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Molecule Type
Protein
Gene Name
TET(44)
Gene ID
66355013
Sequence
MKTNNMKQAILSSATNLIAKNGVQNTSLADIAKDVNISKGTLYYHYASKDDIIYDIADTH
LEVITSAILNCVKNVKSKNSQIEMVNLILEKISTIESRGRVHMYLICEAITSNNDLKERI
RLKYIEWRTTLKSEIVESLEKYNSSENEQDAESFSFLLMSIVDGLVVQSLLKTEKIPYEN
IASFLVNHWI
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Uniprot ID
A0A031WAZ8_CLODI
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Kingdom: N.A.
Phylum: Firmicutes
Class: Clostridia
Order: Eubacteriales
Family: Peptostreptococcaceae
Genus: Clostridioides
Species: Clostridioides difficile
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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Tetracycline
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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: Human immunodeficiency virus infection [1]
Resistant Disease Human immunodeficiency virus infection [ICD-11: 1C62.0]
Resistant Drug Tetracycline
Molecule Alteration Expression
Inherence
Experimental Note Discovered Using In-vivo Testing Model
Mechanism Description Of the resistance mechanisms, C. difficile produces ribosomal protection protein that impedes the attachment of the drug to a ribosome. The TetM protein that functions as ribosomal protectant has been identified in TET-resistant C. difficile strains, whereas the presence of other Tet proteins such as Tet(W) and Tet(44) has also been recognized. The TetM exhibits homology to EF-G and shares the same binding region in a ribosome. The binding of the TetM protein to a ribosome accompanying with the GTP hydrolysis allows conformational change of the ribosome, resulting in the dissociation of TET from its binding site. Cellular protein synthesis is then recovered through the binding of EF-G after the release of hydrolysed TetM.
References
Ref 1 Insights into drug resistance mechanisms in Clostridium difficile .Essays Biochem. 2017 Mar 3;61(1):81-88. doi: 10.1042/EBC20160062. Print 2017 Feb 28. 10.1042/EBC20160062

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