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a mdc1  (Novus Biologicals)
86
Novus Biologicals a mdc1
Figure 7. ATM kinase is a potential therapeutic target for host directed TB therapy. (a) Graphical representation depicting Rv load at day 1 (n = 4) and day 56 (n = 5) of infection in lungs and spleen of mice. Lung homogenates prepared at indicated time points were plated on 7H11 plates to enumerate CFU per lung or per spleen (b) Lung and spleen lysates were prepared from uninfected and Rv infected mice 56 days p.i. 100 mg lung lysates were subjected to immunoblotting with a-gH2AX, a-pATM(S1981) a-ATM, a-pCHK2(T68), a-CHK2, a-pAkt (S473), a-Akt, a-p53 and a-b-actin antibodies. (c) PF were infected with Rv at high MOI (1:10) as described above. 24 h p.i, cells were treated with either 3.6 mM isoniazid (INH) or 10 mM ATM-I alone or INH + ATM-I together. CFUs were enumerated at 24, 48 and 72 hr post treatment. (d) Schematic representation of the mice infection and drug treatment protocol used. (e–f) CFUs were enumerated in lungs of mice at Day 1, and in the lungs (e) and spleen (f) on day 15 and 30 of infection. Number of mice in each batch was 6 (n = 6) except in Rv at Day 1(n = 5). Error bar, SD. *, p0.05; **, p0.005; ***, p0.0005. (g) Model depicting the findings. Rv induces genotoxicity and causes deleterious DSBs in the host genome through SecA2 secretome. Host cell in response to the occurrence of DSBs activate ATM kinase and is recruited at the site of damage by the sensor, MRN complex. Activated ATM autophosphorylates itself and phosphorylates H2AX in the chromatin flanking the sites of DNA damage, which becomes the foundation for the recruitment of mediator protein <t>MDC1,</t> thus amplifying DDR. pATM promote recruitment of 53BP1 at the damage site. pATM as a part of DDR also activates downstream effectors, Chk2 and p53, which are responsible for alterations in the host cell cycle. pATM in a parallel pathway also activates Akt, which is known inhibit apoptosis and promote cell survival. Activation of ATM and Akt and subsequent inhibition of apoptosis provides survival advantage to Rv. Inhibition of ATM or Akt activation through inhibitors, ATM-I or Akt-I, respectively, promote host cell apoptosis, which impedes the bacilli growth. Phosphorylation status of proteins is depicted with a P in a circle. The online version of this article includes the following source data and figure supplement(s) for figure 7:
A Mdc1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/a mdc1/product/Novus Biologicals
Average 86 stars, based on 1 article reviews
a mdc1 - by Bioz Stars, 2026-04
86/100 stars
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mdc1  (Novus Biologicals)
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Novus Biologicals mdc1
Figure 7. ATM kinase is a potential therapeutic target for host directed TB therapy. (a) Graphical representation depicting Rv load at day 1 (n = 4) and day 56 (n = 5) of infection in lungs and spleen of mice. Lung homogenates prepared at indicated time points were plated on 7H11 plates to enumerate CFU per lung or per spleen (b) Lung and spleen lysates were prepared from uninfected and Rv infected mice 56 days p.i. 100 mg lung lysates were subjected to immunoblotting with a-gH2AX, a-pATM(S1981) a-ATM, a-pCHK2(T68), a-CHK2, a-pAkt (S473), a-Akt, a-p53 and a-b-actin antibodies. (c) PF were infected with Rv at high MOI (1:10) as described above. 24 h p.i, cells were treated with either 3.6 mM isoniazid (INH) or 10 mM ATM-I alone or INH + ATM-I together. CFUs were enumerated at 24, 48 and 72 hr post treatment. (d) Schematic representation of the mice infection and drug treatment protocol used. (e–f) CFUs were enumerated in lungs of mice at Day 1, and in the lungs (e) and spleen (f) on day 15 and 30 of infection. Number of mice in each batch was 6 (n = 6) except in Rv at Day 1(n = 5). Error bar, SD. *, p0.05; **, p0.005; ***, p0.0005. (g) Model depicting the findings. Rv induces genotoxicity and causes deleterious DSBs in the host genome through SecA2 secretome. Host cell in response to the occurrence of DSBs activate ATM kinase and is recruited at the site of damage by the sensor, MRN complex. Activated ATM autophosphorylates itself and phosphorylates H2AX in the chromatin flanking the sites of DNA damage, which becomes the foundation for the recruitment of mediator protein <t>MDC1,</t> thus amplifying DDR. pATM promote recruitment of 53BP1 at the damage site. pATM as a part of DDR also activates downstream effectors, Chk2 and p53, which are responsible for alterations in the host cell cycle. pATM in a parallel pathway also activates Akt, which is known inhibit apoptosis and promote cell survival. Activation of ATM and Akt and subsequent inhibition of apoptosis provides survival advantage to Rv. Inhibition of ATM or Akt activation through inhibitors, ATM-I or Akt-I, respectively, promote host cell apoptosis, which impedes the bacilli growth. Phosphorylation status of proteins is depicted with a P in a circle. The online version of this article includes the following source data and figure supplement(s) for figure 7:
Mdc1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mdc1/product/Novus Biologicals
Average 86 stars, based on 1 article reviews
mdc1 - by Bioz Stars, 2026-04
86/100 stars
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anti mdc1  (Novus Biologicals)
86
Novus Biologicals anti mdc1
Figure 7. ATM kinase is a potential therapeutic target for host directed TB therapy. (a) Graphical representation depicting Rv load at day 1 (n = 4) and day 56 (n = 5) of infection in lungs and spleen of mice. Lung homogenates prepared at indicated time points were plated on 7H11 plates to enumerate CFU per lung or per spleen (b) Lung and spleen lysates were prepared from uninfected and Rv infected mice 56 days p.i. 100 mg lung lysates were subjected to immunoblotting with a-gH2AX, a-pATM(S1981) a-ATM, a-pCHK2(T68), a-CHK2, a-pAkt (S473), a-Akt, a-p53 and a-b-actin antibodies. (c) PF were infected with Rv at high MOI (1:10) as described above. 24 h p.i, cells were treated with either 3.6 mM isoniazid (INH) or 10 mM ATM-I alone or INH + ATM-I together. CFUs were enumerated at 24, 48 and 72 hr post treatment. (d) Schematic representation of the mice infection and drug treatment protocol used. (e–f) CFUs were enumerated in lungs of mice at Day 1, and in the lungs (e) and spleen (f) on day 15 and 30 of infection. Number of mice in each batch was 6 (n = 6) except in Rv at Day 1(n = 5). Error bar, SD. *, p0.05; **, p0.005; ***, p0.0005. (g) Model depicting the findings. Rv induces genotoxicity and causes deleterious DSBs in the host genome through SecA2 secretome. Host cell in response to the occurrence of DSBs activate ATM kinase and is recruited at the site of damage by the sensor, MRN complex. Activated ATM autophosphorylates itself and phosphorylates H2AX in the chromatin flanking the sites of DNA damage, which becomes the foundation for the recruitment of mediator protein <t>MDC1,</t> thus amplifying DDR. pATM promote recruitment of 53BP1 at the damage site. pATM as a part of DDR also activates downstream effectors, Chk2 and p53, which are responsible for alterations in the host cell cycle. pATM in a parallel pathway also activates Akt, which is known inhibit apoptosis and promote cell survival. Activation of ATM and Akt and subsequent inhibition of apoptosis provides survival advantage to Rv. Inhibition of ATM or Akt activation through inhibitors, ATM-I or Akt-I, respectively, promote host cell apoptosis, which impedes the bacilli growth. Phosphorylation status of proteins is depicted with a P in a circle. The online version of this article includes the following source data and figure supplement(s) for figure 7:
Anti Mdc1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti mdc1/product/Novus Biologicals
Average 86 stars, based on 1 article reviews
anti mdc1 - by Bioz Stars, 2026-04
86/100 stars
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Figure 7. ATM kinase is a potential therapeutic target for host directed TB therapy. (a) Graphical representation depicting Rv load at day 1 (n = 4) and day 56 (n = 5) of infection in lungs and spleen of mice. Lung homogenates prepared at indicated time points were plated on 7H11 plates to enumerate CFU per lung or per spleen (b) Lung and spleen lysates were prepared from uninfected and Rv infected mice 56 days p.i. 100 mg lung lysates were subjected to immunoblotting with a-gH2AX, a-pATM(S1981) a-ATM, a-pCHK2(T68), a-CHK2, a-pAkt (S473), a-Akt, a-p53 and a-b-actin antibodies. (c) PF were infected with Rv at high MOI (1:10) as described above. 24 h p.i, cells were treated with either 3.6 mM isoniazid (INH) or 10 mM ATM-I alone or INH + ATM-I together. CFUs were enumerated at 24, 48 and 72 hr post treatment. (d) Schematic representation of the mice infection and drug treatment protocol used. (e–f) CFUs were enumerated in lungs of mice at Day 1, and in the lungs (e) and spleen (f) on day 15 and 30 of infection. Number of mice in each batch was 6 (n = 6) except in Rv at Day 1(n = 5). Error bar, SD. *, p0.05; **, p0.005; ***, p0.0005. (g) Model depicting the findings. Rv induces genotoxicity and causes deleterious DSBs in the host genome through SecA2 secretome. Host cell in response to the occurrence of DSBs activate ATM kinase and is recruited at the site of damage by the sensor, MRN complex. Activated ATM autophosphorylates itself and phosphorylates H2AX in the chromatin flanking the sites of DNA damage, which becomes the foundation for the recruitment of mediator protein MDC1, thus amplifying DDR. pATM promote recruitment of 53BP1 at the damage site. pATM as a part of DDR also activates downstream effectors, Chk2 and p53, which are responsible for alterations in the host cell cycle. pATM in a parallel pathway also activates Akt, which is known inhibit apoptosis and promote cell survival. Activation of ATM and Akt and subsequent inhibition of apoptosis provides survival advantage to Rv. Inhibition of ATM or Akt activation through inhibitors, ATM-I or Akt-I, respectively, promote host cell apoptosis, which impedes the bacilli growth. Phosphorylation status of proteins is depicted with a P in a circle. The online version of this article includes the following source data and figure supplement(s) for figure 7:

Journal: eLife

Article Title: Mycobacterium tuberculosis exploits host ATM kinase for survival advantage through SecA2 secretome

doi: 10.7554/elife.51466

Figure Lengend Snippet: Figure 7. ATM kinase is a potential therapeutic target for host directed TB therapy. (a) Graphical representation depicting Rv load at day 1 (n = 4) and day 56 (n = 5) of infection in lungs and spleen of mice. Lung homogenates prepared at indicated time points were plated on 7H11 plates to enumerate CFU per lung or per spleen (b) Lung and spleen lysates were prepared from uninfected and Rv infected mice 56 days p.i. 100 mg lung lysates were subjected to immunoblotting with a-gH2AX, a-pATM(S1981) a-ATM, a-pCHK2(T68), a-CHK2, a-pAkt (S473), a-Akt, a-p53 and a-b-actin antibodies. (c) PF were infected with Rv at high MOI (1:10) as described above. 24 h p.i, cells were treated with either 3.6 mM isoniazid (INH) or 10 mM ATM-I alone or INH + ATM-I together. CFUs were enumerated at 24, 48 and 72 hr post treatment. (d) Schematic representation of the mice infection and drug treatment protocol used. (e–f) CFUs were enumerated in lungs of mice at Day 1, and in the lungs (e) and spleen (f) on day 15 and 30 of infection. Number of mice in each batch was 6 (n = 6) except in Rv at Day 1(n = 5). Error bar, SD. *, p0.05; **, p0.005; ***, p0.0005. (g) Model depicting the findings. Rv induces genotoxicity and causes deleterious DSBs in the host genome through SecA2 secretome. Host cell in response to the occurrence of DSBs activate ATM kinase and is recruited at the site of damage by the sensor, MRN complex. Activated ATM autophosphorylates itself and phosphorylates H2AX in the chromatin flanking the sites of DNA damage, which becomes the foundation for the recruitment of mediator protein MDC1, thus amplifying DDR. pATM promote recruitment of 53BP1 at the damage site. pATM as a part of DDR also activates downstream effectors, Chk2 and p53, which are responsible for alterations in the host cell cycle. pATM in a parallel pathway also activates Akt, which is known inhibit apoptosis and promote cell survival. Activation of ATM and Akt and subsequent inhibition of apoptosis provides survival advantage to Rv. Inhibition of ATM or Akt activation through inhibitors, ATM-I or Akt-I, respectively, promote host cell apoptosis, which impedes the bacilli growth. Phosphorylation status of proteins is depicted with a P in a circle. The online version of this article includes the following source data and figure supplement(s) for figure 7:

Article Snippet: All cell culture reagents were procured from Thermo fisher scientific Inc or Hyclone. a-gH2AX (2577S), a-ATM (2873S), a-pATR-S428 (2853S), a-pChk1S345 (2348S), a-pChk2-T68 (2661S), a-Chk2 (2662S), a-CHK1(2360), a-ATR (13934), a-pAkt-S473 (9271S), a-Akt (9272S), a-p53BP1-T543 (3428S), a-MRE11(4895S), a-pNbs1-S343 and a-Nbs1 (3002S) antibodies were procured from Cell Signalling Technologies. a-pATM-S1891(ab81292) a 53BP1 (ab36823), a-pMDC1-T4 (ab35967), a-RPA2 (ab2175) and a-p53 (ab28) antibody was procured from Abcam. a-p21 (sc-817), a-b-actin (sc-47778), a-b-tubulin (sc-55529) and a-GAPDH (sc25778) antibodies were purchase from Santacruz Biotechnology. a-DNA-PKcs (SAB4502385), apDNA-PKcs-S2056 (SAB4504169) were purchased from Sigma. a-MDC1 and a-pRPA2-S4/S8 was purchased from Novus Biologicals and HRP conjugated secondary antibodies were purchased from Jackson laboratories. a-MDC1 was purchased from Novus Biologicals.

Techniques: Infection, Western Blot, Activation Assay, Inhibition, Phospho-proteomics