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virB10 |
| Victor ID |
962 |
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Gene Name |
virB10 |
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Sequence Strain (Species/Organism) |
Brucella suis 1330 |
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NCBI Gene ID |
1164497
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NCBI Protein GI |
23499827
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Locus Tag |
BRA0060 |
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Genbank Accession |
AE014292 |
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Protein Accession |
NP_699267 |
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Other Database IDs |
UniProtKB-ID: VIRBA_BRUSU
UniRef100: UniRef100_Q9RPX5
UniRef90: UniRef90_Q2YJ81
UniRef50: UniRef50_Q2YJ81
UniParc: UPI00000DD81F
EMBL: AF141604
EMBL: AE014292
EMBL-CDS: AAD56620.1
EMBL-CDS: AAN33272.1
RefSeq_NT: NC_004311.2
GenomeReviews: AE014292_GR
KEGG: bms:BRA0060
NMPDR: fig|204722.1.peg.2176
TIGR: BRA0060
HOGENOM: HBG365517
OMA: FTHPRET
ProtClustDB: CLSK898650
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Taxonomy ID |
204722
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Chromosome No |
II |
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Gene Starting Position |
57867 |
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Gene Ending Position |
59042 |
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Gene Strand (Orientation) |
- |
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Protein Name |
type IV secretion system protein VirB10 |
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Protein pI |
7.06 |
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Protein Weight |
38805.02 |
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Protein Length |
391 |
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Protein Note |
similar to GP:5929875, and GP:5929875; identified by sequence similarity; putative |
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DNA Sequence |
>gi|56968493:57867-59042 Brucella suis 1330 chromosome chromosome II, complete sequence
GTCACTTCGGTTTGACATCATACACACTCGAAAAATCTAGGTCGCGGGCGATATAGATGCCGATCTCTTC
GCCCTGGTTCTTGTACAGTGTCGGCGGAATGTTGATCGTATCCTTCAAGGCAGTTGAAGCCAGGTTGCTC
GTCGATTCACCTCCGCCGGTATTGAGGTTGATCTGATTTGAACCCCCGCCGCCGACCTTCTGGGTTGCAT
AGCGGCCGAGGGTCTCGATCGTGCTCAACATCAAGGCGCCGCCAAAGCGCTTCCAGAAGTGGGAGTCGAT
GTAGCCGGGCAAGCCTGCCCCGCCCAGGGGGTCGGCGCCTGGAGAGTCGAGATCGATCACGACACCGTTC
GGCGTCTTCACGCGCGTCCACAGGACATAAATGCGAGCCATGCCCTGCTTTACGTTGGCATCATATTCAC
CCGAGATGGTTGAACCGCGCTCAATCAGCAACACCTTGCCGTTATCGCTATACATGTTGCGTGTGACCAC
GCAGGCAGCCATGCCCGGCACCGTCGAATCCAGACGGGTTTGCAGCGCGCAATTGATGATGCTGCCCTTC
GCGAGCAGGAAATCACGGTTGCGCAGAAGGCTCGCCATGCGTGCATCCGTTTGTGTGCCGTGAAGGAGAG
TACCCAGCGATCCAGCATCCTGCTTGGTGTTCTTTTGACTGTCGAGCAGGGCTTGAATGCGCGCATTGGT
CGTTTGAACGACCGTATCACCGGCCGTTTGAGCGTTCGTATCGCCGCTGGACTTGGTGACGACCATCAAC
GCGCTGGCCGACTTGTCCAGTACATCGTCCTTTGCCGGCGTATCATCCGGCAATGGTGGCAGGCTCAGCG
CCGCCGCTGCGGGTTCCGCGATGGGCATGGCTGGGGCCGGTGGCGGGGCTGGTGGTTCTGGTGGTGCTGG
TGGTGGCGGGGGTGGCGGGGGTGGCAGCTTGAAAGTTCGCATCGGAACTGTGCTGGTCTGCACCATCGTC
TTGTCTGAATGGTGATTATTCTCTGCATTGCCCCTCATGTGAAACACGAGCAGCAACAGCAGCACGACGA
TGAAGCCCACGACAAAGAGAAAGAGCAACACCTTGCGGGTGCGGCCGGAGCCGTTTTCGTTCACGGTGGG
TAGGCCACGCTCACCGTCAAGTGTGCCCGGCTGCACCGGAATGTTTTCCTGTGTCA
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Protein Sequence |
>gi|23499827|ref|NP_699267.1| type IV secretion system protein VirB10 [Brucella suis 1330]
MTQENIPVQPGTLDGERGLPTVNENGSGRTRKVLLFLFVVGFIVVLLLLLVFHMRGNAENNHHSDKTMVQ
TSTVPMRTFKLPPPPPPPPPAPPEPPAPPPAPAMPIAEPAAAALSLPPLPDDTPAKDDVLDKSASALMVV
TKSSGDTNAQTAGDTVVQTTNARIQALLDSQKNTKQDAGSLGTLLHGTQTDARMASLLRNRDFLLAKGSI
INCALQTRLDSTVPGMAACVVTRNMYSDNGKVLLIERGSTISGEYDANVKQGMARIYVLWTRVKTPNGVV
IDLDSPGADPLGGAGLPGYIDSHFWKRFGGALMLSTIETLGRYATQKVGGGGSNQINLNTGGGESTSNLA
STALKDTINIPPTLYKNQGEEIGIYIARDLDFSSVYDVKPK
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Molecule Role |
Virulence factor |
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Molecule Role Annotation |
MUTATION: Mutants with polar and nonpolar mutations introduced in irB10 showed different behaviors in mice and in the HeLa cell infection assay, suggesting that virB10 per se is necessary for the correct function of this type IV secretion apparatus (Comerci et al., 2001).
A B. abortus virB10 mutant showed a decrease of intracellular live bacteria comparable to that of the wild-type strain until 4 h after infection, indicating that a functional VirB system is not required for the short-term survival of Brucella inside macrophages. At later time points, the number of live virB10 mutants progressively decreased. Hence, the Brucella virB10 strain did not replicate, but rather was killed. Although the virB10 mutants are capable of short-term survival, they can not evade long-term degradation through fusion with lysosomes (Comerci et al., 2001).
B abortus virB1 and virB10 mutants are unable to persist in mouse spleens after i.p. inoculation, suggest that attenuation in the animal model is due to an inability of these strains to grow intracellularly (Comerci et al., 2001).
A B abortus virB10 mutant lost the ability to multiply in HeLa cells and was not recovered from the spleens of infected BALBc mice (Comerci et al., 2001).
The non polar virB10 mutant was able to block the acquisition of cathepsin D, but was not able to translocate to the replication compartment (Comerci et al., 2001).
The virB10 non-polar mutants were capable of avoiding interactions with the endocytic pathway but , diverging to wild-type Brucella, were unable to reach the endoplasmic reticulum to establish their intracellular replication niche and seemed to be recycled to the cell surface (Comerci et al., 2001). |
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COG
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COG2948U, under U: Intracellular trafficking, secretion, and vesicular transport |
| References |
Comerci et al., 2001: Comerci DJ, MartÃnez-Lorenzo MJ, Sieira R, Gorvel JP, Ugalde RA. Essential role of the VirB machinery in the maturation of the Brucella abortus-containing vacuole. Cellular microbiology. 2001; 3(3); 159-168. [PubMed: 11260139].
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