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p sting  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc p sting
    P Sting, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 346 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+p+sting/Phospho-STING+(Ser365)+Rabbit+mAb/pmc12813888-103-23-25
    Average 97 stars, based on 346 article reviews
    p sting - by Bioz Stars, 2026-09
    97/100 stars

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    Related Articles

    Blocking Assay:

    Article Title: TIA1-mediated stress granules inhibit the neuroinflammation and neurodegeneration after spinal cord injury through LCN2 signaling.
    Article Snippet: The proteins were separated by using 10% sodium dodecyl 254 sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and 255 transferred onto a polyvinylidene fluoride (PVDF) membrane (Merck 256 Millipore). .. After blocking with 5% non-fat dry milk for 1 h, the 257 membranes were incubated with specific primary antibodies: mouse 258 anti-GAPDH (1:1, 000, GB15002-100, Servicebio), mouse anti-MBP 259 (1:1, 000, ab62631, Abcam), mouse anti-β-actin (1:1, 000, GB15001- 260 100, Servicebio), mouse anti-tubulin (1:1, 000, GB15140-100, 261 Servicebio), rabbit anti-G3BP1 (1:2, 000, 13057-2-AP, Proteintech), 262 rabbit anti-G3BP2 (1:2,0 00, 16276-1-AP, Proteintech), rabbit anti- 263 TIA1 (1:1, 000, 12133-2-AP, Proteintech), rabbit anti-Lamin B1(1:1, 264 000, ab16048, Abcam), rabbit anti-p-eIF2α (1:1, 000, 28740-1-AP, 265 Proteintech), rabbit anti-eIF2α (1:1, 000, 11170-1-AP, Proteintech), 266 rabbit anti-LCN2 (1:1, 000, 26991-1-AP, Proteintech), rabbit anti- 267 cGAS (1:1, 000, 26416-1-AP, Proteintech), rabbit anti-p-STING (1:1, 268 000, #72971, CST), rabbit anti-STING (1:2, 000, 19851-1-AP, 269 Proteintech), rabbit anti-p-TBK1 (1:1, 000, #5483, CST), rabbit anti- 270 TBK1(1:1, 000, #3504, CST), rabbit anti-p-IRF3 (1:1, 000, #29047, 271 CST), rabbit anti-IRF3 (1:1, 000, #4302, CST). .. After washing for 3 ACCEPTED MANUSCRIPT AR TIC LE IN PR ES S ARTICLE IN PRESS 12 272 times in TBST, the membranes were then incubated with secondary 273 antibodies at room temperature for 1 h: goat anti-mouse HRP- 274 conjugated secondary antibodies (1:10, 000, A9044, Sigma), goat 275 anti-rabbit HRP-conjugated secondary antibodies (1:10, 000, 276 FDR007, FDbio).

    Incubation:

    Article Title: TIA1-mediated stress granules inhibit the neuroinflammation and neurodegeneration after spinal cord injury through LCN2 signaling.
    Article Snippet: The proteins were separated by using 10% sodium dodecyl 254 sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and 255 transferred onto a polyvinylidene fluoride (PVDF) membrane (Merck 256 Millipore). .. After blocking with 5% non-fat dry milk for 1 h, the 257 membranes were incubated with specific primary antibodies: mouse 258 anti-GAPDH (1:1, 000, GB15002-100, Servicebio), mouse anti-MBP 259 (1:1, 000, ab62631, Abcam), mouse anti-β-actin (1:1, 000, GB15001- 260 100, Servicebio), mouse anti-tubulin (1:1, 000, GB15140-100, 261 Servicebio), rabbit anti-G3BP1 (1:2, 000, 13057-2-AP, Proteintech), 262 rabbit anti-G3BP2 (1:2,0 00, 16276-1-AP, Proteintech), rabbit anti- 263 TIA1 (1:1, 000, 12133-2-AP, Proteintech), rabbit anti-Lamin B1(1:1, 264 000, ab16048, Abcam), rabbit anti-p-eIF2α (1:1, 000, 28740-1-AP, 265 Proteintech), rabbit anti-eIF2α (1:1, 000, 11170-1-AP, Proteintech), 266 rabbit anti-LCN2 (1:1, 000, 26991-1-AP, Proteintech), rabbit anti- 267 cGAS (1:1, 000, 26416-1-AP, Proteintech), rabbit anti-p-STING (1:1, 268 000, #72971, CST), rabbit anti-STING (1:2, 000, 19851-1-AP, 269 Proteintech), rabbit anti-p-TBK1 (1:1, 000, #5483, CST), rabbit anti- 270 TBK1(1:1, 000, #3504, CST), rabbit anti-p-IRF3 (1:1, 000, #29047, 271 CST), rabbit anti-IRF3 (1:1, 000, #4302, CST). .. After washing for 3 ACCEPTED MANUSCRIPT AR TIC LE IN PR ES S ARTICLE IN PRESS 12 272 times in TBST, the membranes were then incubated with secondary 273 antibodies at room temperature for 1 h: goat anti-mouse HRP- 274 conjugated secondary antibodies (1:10, 000, A9044, Sigma), goat 275 anti-rabbit HRP-conjugated secondary antibodies (1:10, 000, 276 FDR007, FDbio).

    Article Title: P2X7 receptor-mediated cGAS-STING pathway activation underlies chronic stress-induced depressive-like behaviors.
    Article Snippet: .. Frozen sections were blocked in 5% donkey serum or goat serum in PBS containing 0.3% Triton X-100 at room temperature for 1 h. Thereafter, brain sections were incubated at 4 °C overnight with the following primary antibodies: mouse anti-P2X7 (1:100, #sc-514962, Santa Cruz, USA), rabbit anti-p-STING (1:100, #62,912, CST, USA), rabbit antiIBA1 (1:200, #17,198, CST, USA), goat anti-IBA1 (1:200, #ab5076, Abcam, UK), rabbit anti-GFAP (1:200, #12,389, CST, USA), mouse anti-GFAP (1:200, #3679, CST, USA), rabbit anti-NeuN (1:400, #ab190565, Abcam, UK), mouse anti-NeuN (1:400, #ab104224, Abcam, UK). .. The sections were then washed in PBS and incubated at room temperature for 1 h with the following secondary antibodies: Alexa594-conjugated donkey anti-rabbit IgG, Alexa-488-conjugated donkey anti-mouse IgG, Alexa-594-conjugated donkey anti-mouse IgG, Alexa-488-conjugated donkey anti-rabbit IgG (1:500; Invitrogen, USA).

    other:


    Article Title: STING is the scaffold protein for stress granule pre-condensation at the ER.
    Article Snippet: Rabbit anti-STING (Cat# 13647), rabbit anti-p-STING (Cat# 19781), rabbit anti-TBK1 (Cat# 3504), rabbit anti-p-TBK1 (Cat # 5483), rabbit anti-IRF3 (Cat #4302), rabbit anti-p-IRF3 (Cat #4947), rabbit anti β-ACTIN (Cat# 4970), rabbit anti-eIF4G (Cat# 2498), rabbit anti-caspase-3 (Cat# 9662), rabbit antiFlag (Cat# 14793), rabbit anti-HA (Cat# 3724), rabbit anti-Myc tag (Cat# 2278), rabbit anti-eIF2α (Cat# 5324), rabbit anti-p-eIF2α (Cat# 3398), rabbit anti-histone H3 (Cat# 9715) and rabbit anti-UBAP2L (Cat# 40199) were purchased from Cell Signaling Technology (USA).




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    A. Diagram of the Canonical and Non-canonical STING signaling (created with BioRender.com ). B. Constitutive STAT3 and STAT1 activation in SAVI iECs. Phospho-STAT3 Y705 and phospho-STAT1 Y701 (normalized to total protein) were measured in iECs from 3 HC and 3 SAVI donors across passages 1, 3, and 5. SAVI iECs showed increased baseline STAT3 activation (mean ± SEM; ***p < 0.001, **p < 0.01, *p < 0.05, unpaired t-test). C. <t>STING/TBK1</t> inhibition blocks acute cGAMP-induced STAT3 activation in HC iECs. iECs from 3 HC donors were stimulated with 2’3’-cGAMP (20µg/ml) for 30 min–24 h. STING inhibitor IFM35883 (STINGi, 2.5 μM) and TBK1 inhibitor MRT67307 (TBK1i, 5 μM) were pre-treated one hour before cGAMP. STAT3 activation at 4h was prevented by STING/TBK1 inhibition (mean ±SEM, ***p < 0.001, **p < 0.01, Mann-Whitney test). D. STING/TBK1 inhibition reduces constitutive STAT3 activation in SAVI iECs. SAVI iECs were treated with IFM35883 (2.5 μM) from P2–P5 or with TBK1i (5 μM) for 48 h. Quantification is from four experiments in iEC line from patient SAVI1 (mean ±SEM, ***p < 0.001, unpaired t-test). E. STAT3 shRNA knockdown (KD), not STAT1 KD preserves CD144 (VE-cadherin) in SAVI iECs. iECs from 3 individual SAVI patients infected with control, STAT3, or STAT1 shRNA at P2 were analyzed by flow cytometry at P5 (mean ±SEM, **p < 0.01, paired t-test). Representative flow cytometry profiles are shown in Figure S4C. F. Constitutive protein expression of SLUG/ SNAI2 is elevated in SAVI iECs and suppressed by STING inhibition. Protein from 3 HC, 3 SAVI, and 3 iso-SAVI iECs at P5 showed increased SLUG (normalized by GAPDH) in SAVI; IFM35883 (2.5 μM) treatment from P2–P5 prevented SLUG upregulation in SAVI iECs (SAVI 1) (mean ±SEM, ***p < 0.001, **p < 0.01, unpaired t-test). See also Figure S4E. G. STAT3 shRNA knockdown reduces SLUG mRNA expression (normalized by internal control 18S) in SAVI iECs at P3. Data are summarized from 3 individual SAVI patients iEC lines. *p < 0.01 as determined by two-tailed unpaired t-test.
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    A. Diagram of the Canonical and Non-canonical STING signaling (created with BioRender.com ). B. Constitutive STAT3 and STAT1 activation in SAVI iECs. Phospho-STAT3 Y705 and phospho-STAT1 Y701 (normalized to total protein) were measured in iECs from 3 HC and 3 SAVI donors across passages 1, 3, and 5. SAVI iECs showed increased baseline STAT3 activation (mean ± SEM; ***p < 0.001, **p < 0.01, *p < 0.05, unpaired t-test). C. <t>STING/TBK1</t> inhibition blocks acute cGAMP-induced STAT3 activation in HC iECs. iECs from 3 HC donors were stimulated with 2’3’-cGAMP (20µg/ml) for 30 min–24 h. STING inhibitor IFM35883 (STINGi, 2.5 μM) and TBK1 inhibitor MRT67307 (TBK1i, 5 μM) were pre-treated one hour before cGAMP. STAT3 activation at 4h was prevented by STING/TBK1 inhibition (mean ±SEM, ***p < 0.001, **p < 0.01, Mann-Whitney test). D. STING/TBK1 inhibition reduces constitutive STAT3 activation in SAVI iECs. SAVI iECs were treated with IFM35883 (2.5 μM) from P2–P5 or with TBK1i (5 μM) for 48 h. Quantification is from four experiments in iEC line from patient SAVI1 (mean ±SEM, ***p < 0.001, unpaired t-test). E. STAT3 shRNA knockdown (KD), not STAT1 KD preserves CD144 (VE-cadherin) in SAVI iECs. iECs from 3 individual SAVI patients infected with control, STAT3, or STAT1 shRNA at P2 were analyzed by flow cytometry at P5 (mean ±SEM, **p < 0.01, paired t-test). Representative flow cytometry profiles are shown in Figure S4C. F. Constitutive protein expression of SLUG/ SNAI2 is elevated in SAVI iECs and suppressed by STING inhibition. Protein from 3 HC, 3 SAVI, and 3 iso-SAVI iECs at P5 showed increased SLUG (normalized by GAPDH) in SAVI; IFM35883 (2.5 μM) treatment from P2–P5 prevented SLUG upregulation in SAVI iECs (SAVI 1) (mean ±SEM, ***p < 0.001, **p < 0.01, unpaired t-test). See also Figure S4E. G. STAT3 shRNA knockdown reduces SLUG mRNA expression (normalized by internal control 18S) in SAVI iECs at P3. Data are summarized from 3 individual SAVI patients iEC lines. *p < 0.01 as determined by two-tailed unpaired t-test.
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    Image Search Results


    A. Diagram of the Canonical and Non-canonical STING signaling (created with BioRender.com ). B. Constitutive STAT3 and STAT1 activation in SAVI iECs. Phospho-STAT3 Y705 and phospho-STAT1 Y701 (normalized to total protein) were measured in iECs from 3 HC and 3 SAVI donors across passages 1, 3, and 5. SAVI iECs showed increased baseline STAT3 activation (mean ± SEM; ***p < 0.001, **p < 0.01, *p < 0.05, unpaired t-test). C. STING/TBK1 inhibition blocks acute cGAMP-induced STAT3 activation in HC iECs. iECs from 3 HC donors were stimulated with 2’3’-cGAMP (20µg/ml) for 30 min–24 h. STING inhibitor IFM35883 (STINGi, 2.5 μM) and TBK1 inhibitor MRT67307 (TBK1i, 5 μM) were pre-treated one hour before cGAMP. STAT3 activation at 4h was prevented by STING/TBK1 inhibition (mean ±SEM, ***p < 0.001, **p < 0.01, Mann-Whitney test). D. STING/TBK1 inhibition reduces constitutive STAT3 activation in SAVI iECs. SAVI iECs were treated with IFM35883 (2.5 μM) from P2–P5 or with TBK1i (5 μM) for 48 h. Quantification is from four experiments in iEC line from patient SAVI1 (mean ±SEM, ***p < 0.001, unpaired t-test). E. STAT3 shRNA knockdown (KD), not STAT1 KD preserves CD144 (VE-cadherin) in SAVI iECs. iECs from 3 individual SAVI patients infected with control, STAT3, or STAT1 shRNA at P2 were analyzed by flow cytometry at P5 (mean ±SEM, **p < 0.01, paired t-test). Representative flow cytometry profiles are shown in Figure S4C. F. Constitutive protein expression of SLUG/ SNAI2 is elevated in SAVI iECs and suppressed by STING inhibition. Protein from 3 HC, 3 SAVI, and 3 iso-SAVI iECs at P5 showed increased SLUG (normalized by GAPDH) in SAVI; IFM35883 (2.5 μM) treatment from P2–P5 prevented SLUG upregulation in SAVI iECs (SAVI 1) (mean ±SEM, ***p < 0.001, **p < 0.01, unpaired t-test). See also Figure S4E. G. STAT3 shRNA knockdown reduces SLUG mRNA expression (normalized by internal control 18S) in SAVI iECs at P3. Data are summarized from 3 individual SAVI patients iEC lines. *p < 0.01 as determined by two-tailed unpaired t-test.

    Journal: bioRxiv

    Article Title: STING–STAT3–SOX18 Axis Drives EndMT and Epigenetic Reprogramming in SAVI Lung Fibrosis

    doi: 10.64898/2026.03.23.713256

    Figure Lengend Snippet: A. Diagram of the Canonical and Non-canonical STING signaling (created with BioRender.com ). B. Constitutive STAT3 and STAT1 activation in SAVI iECs. Phospho-STAT3 Y705 and phospho-STAT1 Y701 (normalized to total protein) were measured in iECs from 3 HC and 3 SAVI donors across passages 1, 3, and 5. SAVI iECs showed increased baseline STAT3 activation (mean ± SEM; ***p < 0.001, **p < 0.01, *p < 0.05, unpaired t-test). C. STING/TBK1 inhibition blocks acute cGAMP-induced STAT3 activation in HC iECs. iECs from 3 HC donors were stimulated with 2’3’-cGAMP (20µg/ml) for 30 min–24 h. STING inhibitor IFM35883 (STINGi, 2.5 μM) and TBK1 inhibitor MRT67307 (TBK1i, 5 μM) were pre-treated one hour before cGAMP. STAT3 activation at 4h was prevented by STING/TBK1 inhibition (mean ±SEM, ***p < 0.001, **p < 0.01, Mann-Whitney test). D. STING/TBK1 inhibition reduces constitutive STAT3 activation in SAVI iECs. SAVI iECs were treated with IFM35883 (2.5 μM) from P2–P5 or with TBK1i (5 μM) for 48 h. Quantification is from four experiments in iEC line from patient SAVI1 (mean ±SEM, ***p < 0.001, unpaired t-test). E. STAT3 shRNA knockdown (KD), not STAT1 KD preserves CD144 (VE-cadherin) in SAVI iECs. iECs from 3 individual SAVI patients infected with control, STAT3, or STAT1 shRNA at P2 were analyzed by flow cytometry at P5 (mean ±SEM, **p < 0.01, paired t-test). Representative flow cytometry profiles are shown in Figure S4C. F. Constitutive protein expression of SLUG/ SNAI2 is elevated in SAVI iECs and suppressed by STING inhibition. Protein from 3 HC, 3 SAVI, and 3 iso-SAVI iECs at P5 showed increased SLUG (normalized by GAPDH) in SAVI; IFM35883 (2.5 μM) treatment from P2–P5 prevented SLUG upregulation in SAVI iECs (SAVI 1) (mean ±SEM, ***p < 0.001, **p < 0.01, unpaired t-test). See also Figure S4E. G. STAT3 shRNA knockdown reduces SLUG mRNA expression (normalized by internal control 18S) in SAVI iECs at P3. Data are summarized from 3 individual SAVI patients iEC lines. *p < 0.01 as determined by two-tailed unpaired t-test.

    Article Snippet: After blocking with LI-COR blocking buffer, the membranes were incubated with primary antibodies for VE-cadherin (1:1000, CST, Cat#2500S), CD31(1:1000, DAKO, Cat#M0823), SMA (1:2000, Abcam, Cat#ab7817), SM22 (1:1000, Abcam, Cat#ab14106), SOX18 (1:100, Santa Cruz, Cat#sc-166025), SLUG (1:1000, CST, Cat#9585S), P-STAT3 Y705 (1:1000, CST, Cat#9145S), STAT3 (1:1000, CST, Cat#9139S), P-STAT1 Y701 (1:1000, CST, Cat#9167S), STAT1(1:1000, CST, Cat#9172S), P-STING S366 (1:1000, CST, Cat#19781S), STING (1:1000, CST, Cat#13647S), P-TBK1 S172 (1:1000, CST, Cat#5483S), TBK1 (1:1000, CST, Cat#3504S), P-IRF3 S396 (1:1000, CST, Cat#4947S), and IRF3 (1:1000, CST, Cat#11904S) overnight at 4°C; these antibodies are listed in the Key Resource table.

    Techniques: Activation Assay, Inhibition, MANN-WHITNEY, shRNA, Knockdown, Infection, Control, Flow Cytometry, Expressing, Two Tailed Test