Molecule Information
General Information of the Molecule (ID: Mol04391)
| Name |
CRISPR system Cms protein Csm4 (csm4)
,Homo sapiens
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| Synonyms |
CRISPR type III-A associated RAMP protein Csm4
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| Molecule Type |
Protein
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| Gene Name |
csm4
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| Gene ID | |||||
| Sequence |
MNSRLFRFDFDRTHFGDHGLESSTISCPADTLYSALCVEALRMGGQQLLGELVACSTLRL
TDLLPYVGPDYLVPKPLHSVRSDGSSMQKKLAKKIGFLPAAQLGSFLDGTADLKELAAR Q TKIGVHAVSAKAAIHNGKKDADPYRVGYFRFELDAGLWLLATGSESELGLLTRLLKGI SA LGGERTSGFGAFNLTESEAPAALTPTVDAASLMTLTTSLPTDDELEAALAGATYRLV KRS GFVASSTYADMPLRKRDIYKFAAGSVFSRPFQGGILDVSLGGNHPVYSYARPLFLA LPES AA Click to Show/Hide
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| Function |
CRISPR is an adaptive immune system that provides protection againstmobile genetic elements . CRISPR clusters contain spacers, sequences complementary toantecedent mobile elements, and target invading nucleic acids. CRISPRclusters are transcribed and processed into CRISPR RNA . Thetype III-A Csm effector complex binds crRNA and acts as a crRNA-guidedRNase, DNase and cyclic oligoadenylate synthase; binding of target RNAcognate to the crRNA is required for all activities . ThisCRISPR-Cas system protects bacteria against transformation withplasmids containing DNA homologous to its spacer regions. {ECO:0000269|PubMed:29979631,ECO:0000305|PubMed:29979631}.; The subunit probably binds to the 5' handle of the crRNA,helping in discrimination between self- and non-self.{ECO:0000250|UniProtKB:A0A0A7HGA1}.
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| Uniprot ID | |||||
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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: Tuberculosis [ICD-11: 1B10.0] | [1] | |||
| Resistant Disease | Tuberculosis [ICD-11: 1B10.0] | |||
| Resistant Drug | Capreomycin | |||
| Molecule Alteration | Mutation | K444R/E+N450D |
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| In Vitro Model | L6TG Cap cells | N.A. | Homo sapiens (Human) | CVCL_C566 |
| Experiment for Drug Resistance |
MIC assay; Time-Kill assay | |||
| Mechanism Description | We found that, the?rv2820c?K114N mutation was highly enriched in CAP-resistant?Mtb?clinical isolates, especially in those isolates with the known CAP resistance conferring mutation?rrs?A1401G, implying the association of this mutation with the antimycobacterial efficacy of CAP. Subsequently, over-expressing the?rv2820c?K114N mutant was shown to increase the tolerance to CAP in?Ms, implying that the?rv2820c?K114N mutation might also confer tolerance to CAP in?Mtb?and be considered as a potential molecular marker for CAP tolerance in?Mtb?clinical isolates. | |||
References
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