Tpca 1

Manufactured by Cayman Chemical

Sourced in United States

TPCA-1 is a small molecule that acts as a potent and selective inhibitor of the PARP14 enzyme. It is a research tool commonly used in studies related to inflammation and immune responses.

Automatically generated - may contain errors

Lab products found in correlation

Cell counting kit 8 (cck8), by Dojindo Laboratories (1 mentions) Lps rs, by InvivoGen (1 mentions) Versamax microplate reader, by Molecular Devices (1 mentions) Aeb071, by MedChemExpress (1 mentions) G 6976, by Enzo Life Sciences (1 mentions) Bay11 7082, by R&D Systems (1 mentions) Mg132, by Thermo Fisher Scientific (1 mentions) Phorbol myristate acetate (pma), by Thermo Fisher Scientific (1 mentions) G 6983, by Cayman Chemical (1 mentions) N acetyl cysteine (nac), by Merck Group (1 mentions) Dmi4000 inverted microscope, by Leica (1 mentions) Tpca 1, by Abcam (1 mentions) Bay 11 7082, by Cayman Chemical (1 mentions) Mg132, by Abcam (1 mentions) Oxaliplatin, by Fujifilm (1 mentions) Curcumin, by Fujifilm (1 mentions) Bay 11 7082, by Abcam (1 mentions) Mg132, by Cayman Chemical (1 mentions)

5 protocols using tpca 1

Endometrial Cell Proliferation Assay

Check if the same lab product or an alternative is used in the 5 most similar protocols

Endometrial cells were seeded in 6-well tissue culture plates at a density of 1 × 10⁵ cells per well. The culture medium was changed to DMEM/F12 with 2% FBS after 24 h of incubation. After changing the media, endometrial cells were treated with rHMGB-1 (Sino, Beijing, China) at a concentration of 15 ng/mL for 12, 24, or 48 h or treated with rHMGB-1 at concentrations of 0, 5, 10, or 15 ng/mL for 48 h. For suppression of TLR4, endometrial cells were treated with 100 ng/mL LPS-RS (InvivoGen, San Diego, CA, USA) for 30 min. For suppression of NF-κB, endometrial cells were treated with 2 μM TPCA-1 (Cayman, Ann Arbor, MI, USA) for 1 h. Both treatments were followed by rHMGB-1 treatment at concentrations of 0, 5, 10, or 15 ng/mL for 48 h. Thereafter, 100 μL of CCK-8 (Cell Counting Kit-8; Dojindo, Japan) was added to each well, and plates were incubated at 37°C for 1 h. Supernatants were transferred to 96-well plates after incubation, and the OD was measured at 450 nm using a VersaMax microplate reader (Molecular Devices) to measure cell proliferation rates.

Yun B.H., Chon S.J., Choi Y.S., Cho S., Lee B.S, & Seo S.K. (2016). Pathophysiology of Endometriosis: Role of High Mobility Group Box-1 and Toll-Like Receptor 4 Developing Inflammation in Endometrium. PLoS ONE, 11(2), e0148165.

+ Open protocol

+ Expand

Investigating PMA-Induced Signaling Pathways

Check if the same lab product or an alternative is used in the 5 most similar protocols

2.5 × 10⁵ cells were plated in a 6-well plate 1 day prior to drug treatment. PMA was then added to the media and incubated at 37°C with 5% CO₂ for 6 hours unless otherwise indicated. For experiments utilizing inhibitors, cells were pretreated with inhibitors 30 minutes prior to PMA induction (25ng/mL). PMA (Fisher Scientific), cyclohexamide (Acros Organics), Gö6983 (Cayman Chemical), LY294002 (EMD Chemicals), UO126 (EMD Chemicals), BIM-1 (Cayman Chemical), Gö6976 (Enzo Life Sciences), AEB071 (Medchem Express), BAY 11-7082 (R&D Systems), MG132 (Fisher Scientific), and TPCA-1 (Cayman Chemical) were stored as recommended.

Leonard B., McCann J.L., Starrett G.J., Kosyakovsky L., Luengas E.M., Molan A.M., Burns M.B., McDougle R.M., Parker P.J., Brown W.L, & Harris R.S. (2015). The PKC-NFκB Signaling Pathway Induces APOBEC3B Expression in Multiple Human Cancers. Cancer research, 75(21), 4538-4547.

+ Open protocol

+ Expand

Recombinant Enzyme Assays for IKKβ, IκBα, PFKFB3, and c-JUN

Check if the same lab product or an alternative is used in the 5 most similar protocols

Recombinant active GST- IKKβ (31176) was purchased from Active Motif. Recombinant GST-IκBα (I20-30G), GST-PFKFB3 (P323-30G), GST-PFKFB3 S269A (custom order), and GST-PFKFB4 (P324-30G) were purchased from SignalChem. Recombinant GST-c-JUN (GLO127G) was purchased from GloboZymes. and adenosine 5′-triphosphate, [γ-32P]-(BLU5024) was purchased from PerkinElmer. Bay (10010266) and TPCA-1 (15115) were purchased from Cayman Chemical. 6-dizao-5-oxo-L-norleucine (D2141), dimethyl succinate (W239607CSBOLDSTART),CSBOLDEND and NAC (138061) were purchased from Sigma. LPS serotype 0111:B4 (ALX-581-012-L001) was purchased from Enzo Life Sciences. GSH monoethyl ester (353905) was purchased from Calbiochem. pLX304 (25890), pLPC-N-Flag (12521), pLKO.1-Scramble (1864), pCMV2-Flag-IKKβ (11103), pCMV2-Flag-IKKβ kinase iNACtive (11104), and pBabe-Puro-IKBα-mut (15291) were purchased from Addgene. pLX304-PFKFB3 was purchased from Thermo-Dharmacon. pLX304-PFKFB3 S269A and S269D mutants were generated by MCLab. TRC human p65 shRNA (TRCN0000014686), TRC human IKKβ shRNA (TRCN0000 018917), and TRC human PFKFB3 shRNA (TRCN0000007338) plasmids were purchased from Thermo-Dharmacon.

Reid M.A., Lowman X.H., Pan M., Tran T.Q., Warmoes M.O., Ishak Gabra M.B., Yang Y., Locasale J.W, & Kong M. (2016). IKKβ promotes metabolic adaptation to glutamine deprivation via phosphorylation and inhibition of PFKFB3. Genes & Development, 30(16), 1837-1851.

+ Open protocol

+ Expand

Migratory Potential of B16F10 and MDA-MB-231 Cells

Check if the same lab product or an alternative is used in the 5 most similar protocols

35,000 B16F10 cells were seeded in 24-well plates in standard culture medium and allowed to grow to confluency for 48 h. The scratch was performed with a sterile p200 pipette tip. The medium was removed and substituted, after one wash in PBS, with phenol red- and serum-free medium, containing the treatment compound at the indicated concentration. For rescue experiments, cells were pre-treated for 1 h with the NF-κB inhibitor TPCA-1 (0.5 μM, Cayman #15115) or the Rho/Rac/Cdc42 Activator I (2.5 μg/ml, Cytoskeleton, Inc. #CN-04A) before performing the scratch. The inhibitors were present throughout the assay. BNIP-3 was overexpressed 24 h after seeding using the LT-1 transfection reagent (Mirus) (pCI BNIP-3 plasmid was a kind gift from Dr. Vanina Romanello [43 (link)]). BNIP-3 overexpression was confirmed using Western Blot as described above. Images of the same fields were taken 0, 15, 20, and 24 h after performing the scratch with a Leica DMI4000 inverted microscope. The area of the scratch was calculated using ImageJ software. The migration rate is expressed as % of the initial gap area. For MDA-MB-231 cells, 40,000 cells were seeded in 24-well plates. Cells were serum-starved for 8 h prior to performing the scratch, after which the medium was substituted with phenol-red free medium containing 2% FBS. Treatment, transfection, and co-treatments were performed as described above.

Bachmann M., Rossa A., Varanita T., Fioretti B., Biasutto L., Milenkovic S., Checchetto V., Peruzzo R., Ahmad S.A., Patel S.H., Lukowski R., Edwards M.J., Ceccarelli M., Gulbins E., Zoratti M., Mattarei A, & Szabo I. (2022). Pharmacological targeting of the mitochondrial calcium-dependent potassium channel KCa3.1 triggers cell death and reduces tumor growth and metastasis in vivo. Cell Death & Disease, 13(12), 1055.

+ Open protocol

+ Expand

Investigating NF-κB Inhibitors in Oxaliplatin and Curcumin Treatment

Check if the same lab product or an alternative is used in the 5 most similar protocols

Oxaliplatin and curcumin were purchased from FUJIFILM Wako Pure Chemical. Three known NF‐κB inhibitors (Bay11‐7082; IκBα kinase inhibitor, TPCA1; IκB kinase inhibitor, MG132; proteasome inhibitor) were purchased from Abcam for Bay11‐7082 and TPCA1, or from Cayman Chemical for MG132, respectively. CMG was synthesized using a previous method (KNC Laboratories).²¹

Ozawa‐Umeta H., Kishimoto A., Imaizumi A., Hashimoto T., Asakura T., Kakeya H, & Kanai M. (2020). Curcumin β‐D‐glucuronide exhibits anti–tumor effects on oxaliplatin‐resistant colon cancer with less toxicity in vivo. Cancer Science, 111(5), 1785-1793.

+ Open protocol

+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Revolutionizing how scientists
search and build protocols!