Interaction of biotin-cdigmp in Mtb
Ontology highlight
ABSTRACT:
ORGANISM(S): Mycobacterium Tuberculosis H37ra
SUBMITTER: 
Shiyun Chen
PROVIDER: PXD073267 | iProX | Tue Jan 20 00:00:00 GMT 2026
REPOSITORIES: iProX
Similar Datasets
Project description:Identification of DNA-binding proteins interacting with the cas6 promoter in the Mtb Δorn strain
2025-06-24 | PXD065366 |
Project description:Identification of G-quadruplex-interacting Proteins in Living Cells using an artificial G4-targeting Biotin ligase
| PRJNA926896 | ENA
Project description:Mycobacterium tuberculosis (Mtb) antigen-specific cellular response is promising for detectionof Mtb infection, but not efficient for diagnosis of TB. We firstly identified 16 TB disease-specific protein markers measured in the culture supernatant of Mtb-stimulated whole blood using a 640 human proteins array, the highest throughput antibody-based protein array available at the time when we did this study. Potential TB-related proteins were then analyzed across three different patient cohorts comprised of healthy controls, LTBI, non-TB pneumonia, and TB patients to evaluate how the biomarkers performed in diagnosing TB in the real clinical setting. The data finally reveal an eight-protein biosignature of TB.
2019-06-25 | GSE133249 | GEO
Project description:Mycobacterium tuberculosis (Mtb) antigen-specific cellular response is promising for detectionof Mtb infection, but not efficient for diagnosis of TB. We firstly identified 16 TB disease-specific protein markers measured in the culture supernatant of Mtb-stimulated whole blood using a 640 human proteins array, the highest throughput antibody-based protein array available at the time when we did this study. Potential TB-related proteins were then analyzed across three different patient cohorts comprised of healthy controls, LTBI, non-TB pneumonia, and TB patients to evaluate how the biomarkers performed in diagnosing TB in the real clinical setting. The data finally reveal an eight-protein biosignature of TB.
2019-12-12 | GSE141848 | GEO
Project description:Mycobacterium tuberculosis (Mtb) is the causative agent of tuberculosis, the leading cause of death among all infectious diseases. There are 11 eukaryotic-like serine/threonine protein kinases (STPKs) in Mtb, which are thought to play pivotal roles in cell growth, signal transduction and pathogenesis. However, their underlying mechanisms of action remain largely uncharacterized. In this study, using a Mtb proteome microarray, we have globally identified the binding proteins in Mtb for all of the STPKs, and constructed the first STPK protein interaction (KPI) map that includes 492 binding proteins and 1,027 interactions. Bioinformatics analysis showed that the interacting proteins reflect diverse functions, including roles in two-component system, transcription, protein degradation, and cell wall integrity. Functional investigations confirmed that PknG regulates cell wall integrity through key components of peptidoglycan (PG) biosynthesis, e.g., MurC. The global STPK-KPIs network constructed here is expected to serve as a rich resource for understanding the key signaling pathways in Mtb, thus facilitating drug development and effective control of Mtb.
2017-06-06 | PXD006389 | Pride
Project description:New tuberculosis vaccines are highly desirable and urgently needed since the attenuated Mycobacterium bovis Bacillus Calmette-Guerin (BCG) provides only variable efficacy against the pulmonary form of the disease. The region of difference 1 (RD1), which is deleted in BCG and strongly impacts on Mycobacterium tuberculosis (Mtb) virulence and immunogenicity, represents a crucial locus to be engineered for either the improvement of the current BCG vaccine, or the attenuation of Mtb. Therefore, mutants secreting or not wild-type or mutated variants of the RD1-encoded 6 kDa early secreted antigenic target (ESAT-6) were generated. Comparative analysis of the transcriptome, phenotype, cytokine production profiles and the capacity to promote T cell responses were conducted in human primary dendritic cells (DCs), as they represent critical regulators of vaccine-induced immunity, unveiling a distinct immunogenic potential for BCG or Mtb mutants. In contrast to Mtb, BCG induced a poor DC maturation, and to our surprise, a BCG strain complemented with the RD1 region only partially restored DC maturation and expansion of interferon (IFN)-γ producing T cells. In contrast, infection with a recombinant attenuated Mtb strain, secreting a truncated version of ESAT-6 lacking 11 amino acids at the C-terminus portion, drove full maturation in infected DC and maintained their capacity to promote polarization of T helper (Th) 1 cells, as observed upon infection with the virulent Mtb. We performed a comparative microarray analysis of dendritic cells (DCs), infected with Mtb and BCG strains, expressing/complemented (MtbÎRD1::RD1 and BCG::RD1) or not (MtbÎRD1::B412 and BCG::B412) the/with the RD1 region. DCs were challenged with different BCG and Mtb recombinant strains for 8h.
2016-07-03 | E-GEOD-62423 | biostudies-arrayexpress
Project description:New tuberculosis vaccines are highly desirable and urgently needed since the attenuated Mycobacterium bovis Bacillus Calmette-Guerin (BCG) provides only variable efficacy against the pulmonary form of the disease. The region of difference 1 (RD1), which is deleted in BCG and strongly impacts on Mycobacterium tuberculosis (Mtb) virulence and immunogenicity, represents a crucial locus to be engineered for either the improvement of the current BCG vaccine, or the attenuation of Mtb. Therefore, mutants secreting or not wild-type or mutated variants of the RD1-encoded 6 kDa early secreted antigenic target (ESAT-6) were generated. Comparative analysis of the transcriptome, phenotype, cytokine production profiles and the capacity to promote T cell responses were conducted in human primary dendritic cells (DCs), as they represent critical regulators of vaccine-induced immunity, unveiling a distinct immunogenic potential for BCG or Mtb mutants. In contrast to Mtb, BCG induced a poor DC maturation, and to our surprise, a BCG strain complemented with the RD1 region only partially restored DC maturation and expansion of interferon (IFN)-γ producing T cells. In contrast, infection with a recombinant attenuated Mtb strain, secreting a truncated version of ESAT-6 lacking 11 amino acids at the C-terminus portion, drove full maturation in infected DC and maintained their capacity to promote polarization of T helper (Th) 1 cells, as observed upon infection with the virulent Mtb.
2016-01-01 | GSE62423 | GEO
Project description:Genome-wide identification of H2A.Z-interacting proteins by bPPI-seq
| PRJNA318889 | ENA
Project description:Goal: Assess transcriptional changes in Mtb associated with activation of adenylyl cyclase activity in the bacterium, by treatment with the Rv1625c agonist V-59 or activation of the TetOn-cAMP construct. Specifically, address changes in transcription of cholestrrol utilization genes, during growth of Mtb in cholesterol media. Method: WT, Rv1625c knockout, and Rv1625c Complement strains of Mtb were grown in cholesterol-based media and treated with V-59 or vehicle control (DMSO). V-59 is known to increase cAMP synthesis in WT, but not in Rv1625c knockout Mtb. V-59 increases cAMP synthesis above that observed in WT in the Complement strain, due to Rv1625c overexpression in this strain. Also, utilized TetOn-cAMP Mtb strain, to induce cAMP synthesis independent of V-59 and Rv1625c. Treatment with Atc induces expression of catalytic domain of Rv1264 in this strain. We grew the TetOn-cAMP strain in cholesterol-based media, treated with Atc or EtOH (vehicle control). Conclusions: Transcriptional changes to cholesterol utilization genes associated with V-59 treatment in WT Mtb were similar to those associated with TetOn-cAMP induction. The transcriptional changes associated with blockade of cholesterol degradation following V-59 treatment in WT Mtb were not observed in the Rv1625c knockout strain. The Rv1625c knockout strain had intrinsic defects in induction of cholesterol utilization genes. The Complement strain showed enhanced transcriptional changes in response to V-59 treatment.
2021-12-16 | GSE190875 | GEO