pI: 8.468 |
Length (AA): 639 |
MW (Da): 71258 |
Paralog Number:
0
Signal peptide: N | GPI Anchor: | Predicted trans-membrane segments: 0
Targets have been classified into druggability groups (DG) according to their druggability score in network driven prioritizations. DGs range from 1 to 5; the higher the group number, the higher the chance of the target to be druggable
Modbase 3D models:
PDB Structures:
Upregulation Percent | Ranking | Stage | Dataset |
---|---|---|---|
Upper 60-80% percentile | Bloodstream Form. | Siegel TN |
Upregulation Percent | Ranking | Stage | Dataset |
---|---|---|---|
Mid 40-60% percentile | Procyclic. | Siegel TN |
Siegel TN | Genome-wide analysis of mRNA abundance in two life-cycle stages of Trypanosoma brucei and identification of splicing and polyadenylation sites. |
Ortholog group members (OG5_149332)
Species | Accession | Gene Product |
---|---|---|
Leishmania braziliensis | LbrM.35.5920 | hypothetical protein, conserved |
Leishmania donovani | LdBPK_365890.1 | Cyclin 12, L-type |
Leishmania infantum | LinJ.36.5890 | hypothetical protein, conserved |
Leishmania major | LmjF.36.5640 | hypothetical protein, conserved |
Leishmania mexicana | LmxM.36.5640 | hypothetical protein, conserved |
Trypanosoma brucei gambiense | Tbg972.10.11200 | hypothetical protein, conserved |
Trypanosoma brucei | Tb927.10.9160 | Cyclin 12, L-type |
Trypanosoma congolense | TcIL3000_10_7930 | Cyclin 12, L-type |
Trypanosoma cruzi | TcCLB.503525.20 | Cyclin 12, L-type |
Trypanosoma cruzi | TcCLB.507825.49 | Cyclin 12, L-type |
Gene/Ortholog | Organism | Phenotype | Source Study |
---|---|---|---|
Tb927.10.9160 this record | Trypanosoma brucei | significant loss of fitness in bloodstream forms (3 days) | alsford |
Tb927.10.9160 this record | Trypanosoma brucei | significant loss of fitness in bloodstream forms (6 days) | alsford |
Tb927.10.9160 this record | Trypanosoma brucei | no significant loss or gain of fitness in procyclic forms | alsford |
Tb927.10.9160 this record | Trypanosoma brucei | no significant loss or gain of fitness in differentiation of procyclic to bloodstream forms | alsford |
yeastgenome | Systematic deletion of yeast genes | Saccharomyces Genome Database |
gerdes | Experimental determination and system-level analysis of essential genes in E. coli MG1655 | Gerdes et al., J Bacteriol. 2003 185:5673-84 |
wormbase | C. elegans RNAi experiments | WormBase web site, http://www.wormbase.org, release WS170 |
blattner | Systematic mutagenesis of the E. coli (MG1655) genome | J Bacteriol 2004, 186:4921-4930 |
shigen | Profiling of E. coli Chromosome (PEC) | National Institute of Genetics, Japan |
nmpdr | Genome-scale essentiality datasets from published studies (M. tuberculosis) | National Microbial Pathogen Data Resource |
alsford | High-throughput phenotyping using parallel sequencing of RNA interference targets in the African trypanosome | Genome Res 2011, 21:915-924 |
neb | C. elegans RNAi phenotypes | Data obtained from Wormbase WS150, curated by K. Chaudary and T. Carlow, New England Biolabs |
keio | Systematic single-gene knock-out mutants of E. coli K12 | The Keio Collection |
Affected Entity | Phenotypic quality | Occurs in | Occurs at | Evidence | Observed in | Drugs/Inhibitors |
---|---|---|---|---|---|---|
cell proliferation (GO:0008283) | decreased (PATO:0000468) | bloodstream stage trypomastigotes (PLO:0027) | inferred from RNAi experiment (ECO:0000019) | No drug identifiers listed for this gene. | ||
Annotator: | fernan@iib.unsam.edu.ar. | Comment: | decreased cell proliferation (significant loss of fitness) in bloodstream forms (stage 6 days). | References: | 21363968 | |
cell proliferation (GO:0008283) | normal (PATO:0000461) | procyclic (PLO:0034) | inferred from RNAi experiment (ECO:0000019) | No drug identifiers listed for this gene. | ||
Annotator: | fernan@iib.unsam.edu.ar. | Comment: | normal cell proliferation (no significant loss or gain of fitness) in differentiation of procyclic to bloodstream forms . | References: | 21363968 |
In TDR Targets, information about phenotypes that are caused by drugs, or by genetic manipulation of cells (e.g. gene knockouts or knockdowns) is manually curated from the literature. These descriptions help to describe the potential of the target for drug development. If no information is available for this gene or if the information is incomplete, this may mean that i) the papers containing this information either appeared after the curation effort for this organism was carried out or they were inadvertently missed by curators; or that ii) the curation effort for this organism has not yet started.
In any case, if you have information about papers containing relevant validation data for this target, please contact us.
1 literature reference was collected for this gene.