Bcl10

Manufactured by Santa Cruz Biotechnology

Sourced in United States

Bcl10 is a protein that regulates apoptosis, or programmed cell death. It is involved in the activation of the NF-kappa-B signaling pathway. Bcl10 plays a role in immune and inflammatory responses.

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Lab products found in correlation

6 protocols using bcl10

Platelet Activation and Signaling Pathways

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ADP, MG132 were obtained from Sigma Aldrich (St. Louis, MO). Thrombin, Collagen, stir bars and other disposables were from Chrono-Log (Havertown, PA), and U46619 was obtained from Cayman Chemical (Ann Arbor, MI). The proteasome inhibitor bortezomib (Velcade) was generous gift from Dr. Steven Schwarze (University of Kentucky College of Medicine, Lexington, KY). FITC-conjugated Annexin V, anti—P-selectin, and PAC-1 antibodies were purchased from Cell Signaling Technology, Inc. (Danvers, MA). Antibodies against TAK1, TAB2, CARMA1, MALT1, Bcl10, Ubiquitin, IKKα, IKKβ, IKKγ, VAMP-8, SNAP-23, Syn-11, and pSer/Thr/Tyr from Santa Cruz (Santa Cruz, CA), respectively. Other reagents were of analytical grade.

Karim Z.A., Vemana H.P, & Khasawneh F.T. (2015). MALT1-Ubiquitination Triggers Non-Genomic NF-κB/IKK Signaling upon Platelet Activation. PLoS ONE, 10(3), e0119363.

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Assessing CBM Complex Formation

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CBM complex formation was assessed in whole cell lysates from BMDCs stimulated for 2 hrs with oxLDL or oxLDL-ICs. Cells were lysed in 1× RIPA buffer followed by immunoprecipitation with antibody to MALT1, CARD9, or Bcl10 (Santa Cruz Biotechnology, Dallas, TX). Western blot analysis was performed as described above with anti-CARD9, anti-Bcl-10, and anti-MALT1 (Cell Signaling Technologies).

Rhoads J.P., Lukens J.R., Wilhelm A.J., Moore J.L., Mendez-Fernandez Y., Kanneganti T.D, & Major A.S. (2017). Oxidized Low-Density Lipoprotein Immune Complex Priming of the Nlrp3 Inflammasome Involves TLR and FcγR Cooperation and Is Dependent on CARD9. The Journal of Immunology Author Choice, 198(5), 2105-2114.

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Investigating Immune Cell Signaling Pathways

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The antibodies for CARD9, CD206, CD68, TGF-β, IL-13, IL-4, IL-18, BCL10, MALT1, GAPDH, β-actin and IgG were from Santa Cruz Biotechnology (Santa Cruz, CA, USA), the phospho-Syk antibody sampler kit, NF-κB pathway sampler kit were from Cell Signaling Technology (Beverly, MA, USA); the antibody for F4/80 was from Abcam (Cambridge, MA, USA); and ChemMate TM EnVision System/DAB Detection Kits were from Dako (Glostrup, Denmark). Antibodies for PerCP/Cy5.5-conjugated CD45.2, phycoerythrin (PE)-conjugated F4/80, fluorescein isothiocyanate (FITC)-conjugated F4/80, FITC-conjugated CD206, PE-conjugated CD3, FITC-conjugated CD4, FITC-conjugated CD8 and isotype control were from Biolegend (San Diego, CA, USA). FITC-conjugated IL-10, FITC-conjugated IL-1α and PE-conjugated IL-12 were from eBioscience (San Diego, CA, USA). Piceatannol and BAY61-3606 were from Sigma (St. Louis, MO, USA). Bio-Plex Cytokine Assay Kits were from Bio-Rad Laboratories (Hercules, CA, USA). Neutralizing anti-VEGF Ab and anti-MIG Ab were from R&D Systems (Minneapolis, MN, USA). Neutralizing anti-IL-15 Ab was from Abcam.

Yang M., Shao J.H., Miao Y.J., Cui W., Qi Y.F., Han J.H., Lin X, & Du J. (2014). Tumor cell-activated CARD9 signaling contributes to metastasis-associated macrophage polarization. Cell Death and Differentiation, 21(8), 1290-1302.

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Immunohistochemical Analysis of Gastric Mucosa

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Gastric mucosa was freshly obtained and embedded in paraffin following formalin fixation. Sections with a thickness of 2 μm were prepared, and subsequently, deparaffinization, rehydration, and endogenous peroxidase inactivation were performed according to standard procedures. Immunohistochemical staining was performed using antibodies against PNLIP (sc-374612; Santa Cruz Biotechnology, TX, USA), BCL10 (sc-5273; Santa Cruz Biotechnology), NKX2-1/TTF1 (SP141; Roche Diagnostics, Basel, Switzerland), SFTPB (sc-133143; Santa Cruz Biotechnology), and SFTPC (ab90716; Abcam, Cambridge, UK). Stained sections were independently evaluated by two pathologists.

Takeuchi C., Sato J., Yamamichi N., Kageyama-Yahara N., Sasaki A., Akahane T., Aoki R., Nakajima S., Ito M., Yamamichi M., Liu Y.Y., Sakuma N., Takahashi Y., Sakaguchi Y., Tsuji Y., Sakurai K., Tomida S., Niimi K., Ushijima T, & Fujishiro M. (2023). Marked intestinal trans-differentiation by autoimmune gastritis along with ectopic pancreatic and pulmonary trans-differentiation. Journal of Gastroenterology, 59(2), 95-108.

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Antibody reagents for NF-kB signaling

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The following antibodies were used in this study: BCL10 (rabbit, sc-5611), BCL10 (goat, sc-9560), IKKα (H-744, sc-7218), IKKα/β (H-470, sc-7607), MALT1 (H-300, sc-28246), NEMO (FL-419, sc-8330), RelB (sc-226), Cylindromatosis-1/CYLD1 (E-10, sc-74435) were from Santa Cruz Biotechnology (Santa Monica, CA, USA). IκBα (44D4, #9242), CARD11/CARMA1 (1D12, #4435), GSK3β (27C10, #9315), GSK3α (#9338) were obtained from Cell Signaling (Danvers, MA, USA). ImmunoCult^TM Human CD3/CD28 T cell activator (#10971) was obtained from STEMCELL technologies Inc. (Cologne, Germany). Polyclonal Goat Anti-Mouse Ig (#553998) and Purified Mouse anti-β-catenin (#610154) were obtained from BD Biosciences (San Jose, CA, USA). β-Tubulin (TUB 2.1, #T4026), the GSK3β inhibitors SB216763 (Sigma-Aldrich, #S3442) and SB415286 (Sigma-Aldrich, #S3567), Cycloheximid (Sigma Aldrich, #C7698), and ionomycin (Sigma Aldrich, #I0634) were from Sigma (Sigma-Aldrich, St. Louis, MO, USA). Control siRNA (#SR-CL000-005), GSK3βsiRNA1 (5′-GACUAGAGGGCAGAGUAAAU-3′) and GSK3βsiRNA2 (5′-CCGGGAACAAAUCCGAGAGAU-3′) were obtained from Eurogentec (Liege, Belgium). PMA was purchased (#524400) from Merck (Darmstadt, Germany).

Abd-Ellah A., Voogdt C., Krappmann D., Möller P, & Marienfeld R.B. (2018). GSK3β modulates NF-κB activation and RelB degradation through site-specific phosphorylation of BCL10. Scientific Reports, 8, 1352.

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Histological Analysis of Xenograft Metastasis

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Tissues were fixed in 10% formalin solution for 24 h and transferred to 70% ethanol. Tissues were paraffin embedded, sectioned and rehydrated. Hematoxylin/eosin and periodic Acid–Schiff staining were performed according to basic procedures. Sections were stained with anti-phospho-Erk1/2 (New England Biolabs, Ipswich, MA), anti-Ki67 (abcam, Cambridge, MA), anti-chromogranin A (abcam, Cambridge, MA), anti-cytokeratin 7 (Invitrogen, Rockford, IL), anti-cytokeratin 19 (Cell Signaling Technology, Danvers, MA) and with Trypsin, Bcl10, Mucin4 from Santa Cruz Biotechnology, Santa Cruz, CA. For each time point, histology of four sections separated by 200 µm from at least three individual animals was evaluated. Metastasis quantification: for each mouse, two lobes of the liver and one lung were sliced and embedded in paraffin. Gross and microscopic examination of H&E stained sections was used to identify the percentage of mice with at least one metastasis to the liver and lung.

Doiron B, & DeFronzo R.A. (2017). A novel experimental model for human mixed acinar–ductal pancreatic cancer. Carcinogenesis, 39(2), 180-190.

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