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1,002 results on '"Washington, M."'

2. Identification and multimodal characterization of a specialized epithelial cell type associated with Crohn’s disease

Author

Li, Jia, Simmons, Alan J., Hawkins, Caroline V., Chiron, Sophie, Ramirez-Solano, Marisol A., Tasneem, Naila, Kaur, Harsimran, Xu, Yanwen, Revetta, Frank, Vega, Paige N., Bao, Shunxing, Cui, Can, Tyree, Regina N., Raber, Larry W., Conner, Anna N., Pilat, Jennifer M., Jacobse, Justin, McNamara, Kara M., Allaman, Margaret M., Raffa, Gabriella A., Gobert, Alain P., Asim, Mohammad, Goettel, Jeremy A., Choksi, Yash A., Beaulieu, Dawn B., Dalal, Robin L., Horst, Sara N., Pabla, Baldeep S., Huo, Yuankai, Landman, Bennett A., Roland, Joseph T., Scoville, Elizabeth A., Schwartz, David A., Washington, M. Kay, Shyr, Yu, Wilson, Keith T., Coburn, Lori A., Lau, Ken S., and Liu, Qi

Published
2024
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3. Colitis-induced upregulation of tumor necrosis factor receptor-2 (TNFR2) terminates epithelial regenerative signaling to restore homeostasis.

Author

Sharifkhodaei, Zohreh, Liu, Cambrian, Girish, Nandini, Huang, Ying, Punit, Shivesh, Washington, M, and Polk, Brent

Subjects
Cell biology, Immunology, Molecular biology, Omics, Physiology, Transcriptomics
Abstract

Colonic epithelial repair is a key determinant of health. Repair involves changes in epithelial differentiation, an extensive proliferative response, and upregulation of regeneration-associated fetal-like transcripts, including Ly6a (Sca-1), that represent Yap1 and interferon targets. However, little is known about how this regenerative program terminates and how homeostasis is restored during injury and inflammation. Here we show that, after the initial entry into the regenerative state, the subsequent upregulation of tumor necrosis factor (TNF) receptor 2 (R2, TNFR2, Tnfrsf1b) clears the regenerative signaling and restores homeostatic patterns of epithelial differentiation. Targeted deletion of epithelial TNFR2 in vivo and in colonoid cultures revealed persistent expression of Ly6a, hyperproliferation, and reduced secretory differentiation. Moreover, mice lacking epithelial TNFR2 also failed to complete colon ulcer healing, suggesting that partial resolution of regenerative signaling is essential for the completion of the repair process. These results demonstrate how epithelial cells dynamically leverage a colitis-associated cytokine to choreograph repair.

Published
2023

5. Iron deficiency linked to altered bile acid metabolism promotes Helicobacter pylori-induced inflammation-driven gastric carcinogenesis

Author

Noto, Jennifer M, Piazuelo, M Blanca, Shah, Shailja C, Romero-Gallo, Judith, Hart, Jessica L, Di, Chao, Carmichael, James D, Delgado, Alberto G, Halvorson, Alese E, Greevy, Robert A, Wroblewski, Lydia E, Sharma, Ayushi, Newton, Annabelle B, Allaman, Margaret M, Wilson, Keith T, Washington, M Kay, Calcutt, M Wade, Schey, Kevin L, Cummings, Bethany P, Flynn, Charles R, Zackular, Joseph P, and Peek, Richard M

Subjects
Cancer, Rare Diseases, Digestive Diseases - (Peptic Ulcer), Nutrition, Digestive Diseases, Infectious Diseases, Emerging Infectious Diseases, 2.1 Biological and endogenous factors, Aetiology, 2.2 Factors relating to the physical environment, Oral and gastrointestinal, Animals, Antigens, Bacterial, Bacterial Proteins, Bile Acids and Salts, Carcinogenesis, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Inflammation, Iron Deficiencies, Mice, Stomach Neoplasms, Bacterial infections, Gastric cancer, Gastroenterology, Infectious disease, Mouse models, Medical and Health Sciences, Immunology
Abstract

Gastric carcinogenesis is mediated by complex interactions among Helicobacter pylori, host, and environmental factors. Here, we demonstrate that H. pylori augmented gastric injury in INS-GAS mice under iron-deficient conditions. Mechanistically, these phenotypes were not driven by alterations in the gastric microbiota; however, discovery-based and targeted metabolomics revealed that bile acids were significantly altered in H. pylori-infected mice with iron deficiency, with significant upregulation of deoxycholic acid (DCA), a carcinogenic bile acid. The severity of gastric injury was further augmented when H. pylori-infected mice were treated with DCA, and, in vitro, DCA increased translocation of the H. pylori oncoprotein CagA into host cells. Conversely, bile acid sequestration attenuated H. pylori-induced injury under conditions of iron deficiency. To translate these findings to human populations, we evaluated the association between bile acid sequestrant use and gastric cancer risk in a large human cohort. Among 416,885 individuals, a significant dose-dependent reduction in risk was associated with cumulative bile acid sequestrant use. Further, expression of the bile acid receptor transmembrane G protein-coupled bile acid receptor 5 (TGR5) paralleled the severity of carcinogenic lesions in humans. These data demonstrate that increased H. pylori-induced injury within the context of iron deficiency is tightly linked to altered bile acid metabolism, which may promote gastric carcinogenesis.

Published
2022

7. Molecular cartography uncovers evolutionary and microenvironmental dynamics in sporadic colorectal tumors

Author

Heiser, Cody N., Simmons, Alan J., Revetta, Frank, McKinley, Eliot T., Ramirez-Solano, Marisol A., Wang, Jiawei, Kaur, Harsimran, Shao, Justin, Ayers, Gregory D., Wang, Yu, Glass, Sarah E., Tasneem, Naila, Chen, Zhengyi, Qin, Yan, Kim, William, Rolong, Andrea, Chen, Bob, Vega, Paige N., Drewes, Julia L., Markham, Nicholas O., Saleh, Nabil, Nikolos, Fotis, Vandekar, Simon, Jones, Angela L., Washington, M. Kay, Roland, Joseph T., Chan, Keith S., Schürpf, Thomas, Sears, Cynthia L., Liu, Qi, Shrubsole, Martha J., Coffey, Robert J., and Lau, Ken S.

Published
2023
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8. Hypusination Maintains Intestinal Homeostasis and Prevents Colitis and Carcinogenesis by Enhancing Aldehyde Detoxification

Author

Gobert, Alain P., Smith, Thaddeus M., Latour, Yvonne L., Asim, Mohammad, Barry, Daniel P., Allaman, Margaret M., Williams, Kamery J., McNamara, Kara M., Delgado, Alberto G., Short, Sarah P., Mirmira, Raghavendra G., Rose, Kristie L., Schey, Kevin L., Zagol-Ikapitte, Irene, Coleman, Jeremy S., Boutaud, Olivier, Zhao, Shilin, Piazuelo, M. Blanca, Washington, M. Kay, Coburn, Lori A., and Wilson, Keith T.

Published
2023
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10. Interleukin-23 receptor signaling impairs the stability and function of colonic regulatory T cells

Author

Jacobse, Justin, Brown, Rachel E., Li, Jing, Pilat, Jennifer M., Pham, Ly, Short, Sarah P., Peek, Christopher T., Rolong, Andrea, Washington, M. Kay, Martinez-Barricarte, Ruben, Byndloss, Mariana X., Shelton, Catherine, Markle, Janet G., Latour, Yvonne L., Allaman, Margaret M., Cassat, James E., Wilson, Keith T., Choksi, Yash A., Williams, Christopher S., Lau, Ken S., Flynn, Charles R., Casanova, Jean-Laurent, Rings, Edmond H.H.M., Samsom, Janneke N., and Goettel, Jeremy A.

Published
2023
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11. Eosinophils Exert Antitumorigenic Effects in the Development of Esophageal Squamous Cell Carcinoma

Author

Jacobse, Justin, Aziz, Zaryab, Sun, Lili, Chaparro, Jasmine, Pilat, Jennifer M., Kwag, Aaron, Buendia, Matthew, Wimbiscus, Mae, Nasu, Motomi, Saito, Tsuyoshi, Mine, Shinji, Orita, Hajime, Revetta, Frank, Short, Sarah P., Kay Washington, M., Hiremath, Girish, Gibson, Michael K., Coburn, Lori A., Koyama, Tatsuki, Goettel, Jeremy A., Williams, Christopher S., and Choksi, Yash A.

Published
2023
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15. Protective Role of Spermidine in Colitis and Colon Carcinogenesis

Author

Gobert, Alain P., Latour, Yvonne L., Asim, Mohammad, Barry, Daniel P., Allaman, Margaret M., Finley, Jordan L., Smith, Thaddeus M., McNamara, Kara M., Singh, Kshipra, Sierra, Johanna C., Delgado, Alberto G., Luis, Paula B., Schneider, Claus, Washington, M. Kay, Piazuelo, M. Blanca, Zhao, Shilin, Coburn, Lori A., and Wilson, Keith T.

Published
2022
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16. Differential Cell Susceptibilities to Kras G12D in the Setting of Obstructive Chronic Pancreatitis

Author

Shi, Chanjuan, Pan, Fong Cheng, Kim, Jessica N, Washington, M Kay, Padmanabhan, Chandrasekhar, Meyer, Christian T, Kopp, Janel L, Sander, Maike, Gannon, Maureen, Beauchamp, R Daniel, Wright, Christopher V, and Means, Anna L

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Pancreatic Cancer, Digestive Diseases, Rare Diseases, Genetics, 2.1 Biological and endogenous factors, Aetiology, Acinar Cells, Animals, Carcinogenesis, Carcinoma, Pancreatic Ductal, Cell Transformation, Neoplastic, Disease Models, Animal, Genes, ras, Metaplasia, Mice, Mutation, Pancreatic Neoplasms, Pancreatitis, Chronic, Precancerous Conditions, Proto-Oncogene Proteins p21(ras), Signal Transduction, Cdkn1a, Cell of Origin, Acinar-to-Ductal Metaplasia, Pancreatic Duct Ligation, Biochemistry and cell biology, Clinical sciences
Abstract

Background & aimsActivating mutation of the KRAS gene is common in some cancers, such as pancreatic cancer, but rare in other cancers. Chronic pancreatitis is a predisposing condition for pancreatic ductal adenocarcinoma (PDAC), but how it synergizes with KRAS mutation is not known.MethodsWe used a mouse model to express an activating mutation of Kras in conjunction with obstruction of the main pancreatic duct to recapitulate a common etiology of human chronic pancreatitis. Because the cell of origin of PDAC is not clear, Kras mutation was introduced into either duct cells or acinar cells.ResultsAlthough KrasG12D expression in both cell types was protective against damage-associated cell death, chronic pancreatitis induced p53, p21, and growth arrest only in acinar-derived cells. Mutant duct cells did not elevate p53 or p21 expression and exhibited increased proliferation driving the appearance of PDAC over time.ConclusionsOne mechanism by which tissues may be susceptible or resistant to KRASG12D-initiated tumorigenesis is whether they undergo a p53-mediated damage response. In summary, we have uncovered a mechanism by which inflammation and intrinsic cellular programming synergize for the development of PDAC.

Published
2019

19. Differential pre-malignant programs and microenvironment chart distinct paths to malignancy in human colorectal polyps

Author

Chen, Bob, Scurrah, Cherie’ R., McKinley, Eliot T., Simmons, Alan J., Ramirez-Solano, Marisol A., Zhu, Xiangzhu, Markham, Nicholas O., Heiser, Cody N., Vega, Paige N., Rolong, Andrea, Kim, Hyeyon, Sheng, Quanhu, Drewes, Julia L., Zhou, Yuan, Southard-Smith, Austin N., Xu, Yanwen, Ro, James, Jones, Angela L., Revetta, Frank, Berry, Lynne D., Niitsu, Hiroaki, Islam, Mirazul, Pelka, Karin, Hofree, Matan, Chen, Jonathan H., Sarkizova, Siranush, Ng, Kimmie, Giannakis, Marios, Boland, Genevieve M., Aguirre, Andrew J., Anderson, Ana C., Rozenblatt-Rosen, Orit, Regev, Aviv, Hacohen, Nir, Kawasaki, Kenta, Sato, Toshiro, Goettel, Jeremy A., Grady, William M., Zheng, Wei, Washington, M. Kay, Cai, Qiuyin, Sears, Cynthia L., Goldenring, James R., Franklin, Jeffrey L., Su, Timothy, Huh, Won Jae, Vandekar, Simon, Roland, Joseph T., Liu, Qi, Coffey, Robert J., Shrubsole, Martha J., and Lau, Ken S.

Published
2021
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21. SELENOP modifies sporadic colorectal carcinogenesis and WNT signaling activity through LRP5/6 interactions

Author

Pilat, Jennifer M., Brown, Rachel E., Chen, Zhengyi, Berle, Nathaniel J., Othon, Adrian P., Washington, M. Kay, Anant, Shruti A., Kurokawa, Suguru, Ng, Victoria H., Thompson, Joshua J., Jacobse, Justin, Goettel, Jeremy A., Lee, Ethan, Choksi, Yash A., Lau, Ken S., Short, Sarah P., and Williams, Christopher S.

Subjects
Colorectal cancer -- Development and progression, Selenoproteins -- Physiological aspects -- Health aspects, Membrane proteins -- Physiological aspects -- Health aspects, Wnt proteins -- Physiological aspects -- Health aspects, Health care industry
Abstract

Although selenium deficiency correlates with colorectal cancer (CRC) risk, the roles of the selenium-rich antioxidant selenoprotein P (SELENOP) in CRC remain unclear. In this study, we defined SELENOP's contributions to sporadic CRC. In human single-cell cRNA-Seq (scRNA-Seq) data sets, we discovered that SELENOP expression rose as normal colon stem cells transformed into adenomas that progressed into carcinomas. We next examined the effects of Selenop KO in a mouse adenoma model that involved conditional, intestinal epithelium-specific deletion of the tumor suppressor adenomatous polyposis coli (Ape) and found that Selenop KO decreased colon tumor incidence and size. We mechanistically interrogated SELENOP-driven phenotypes in tumor organoids as well as in CRC and noncancer cell lines. Selenop-KO tumor organoids demonstrated defects in organoid formation and decreases in WNT target gene expression, which could be reversed by SELENOP restoration. Moreover, SELENOP increased canonical WNT signaling activity in noncancer and CRC cell lines. In defining the mechanism of action of SELENOP, we mapped protein-protein interactions between SELENOP and the WNT coreceptors low-density lipoprotein receptor-related proteins 5 and 6 (LRP5/6). Last, we confirmed that SELENOP-LRP5/6 interactions contributed to the effects of SELENOP on WNT activity. Overall, our results position SELENOP as a modulator of the WNT signaling pathway in sporadic CRC., Introduction Both human observational and animal preclinical studies support tumor-protective roles for the micronutrient selenium in the gastrointestinal tract; however, human clinical trials have yet to corroborate these findings (1-7). [...]

Published
2023
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22. Srs2 promotes synthesis-dependent strand annealing by disrupting DNA polymerase δ-extending D-loops.

Author

Liu, Jie, Ede, Christopher, Wright, William D, Gore, Steven K, Jenkins, Shirin S, Freudenthal, Bret D, Todd Washington, M, Veaute, Xavier, and Heyer, Wolf-Dietrich

Subjects
Saccharomyces cerevisiae, DNA Helicases, DNA Polymerase III, Saccharomyces cerevisiae Proteins, DNA, Base Pairing, DNA helicase, S. cerevisiae, biochemistry, chromosomes, crossover avoidance, genes, genome stability, homologous rcombination, Biochemistry and Cell Biology
Abstract

Synthesis-dependent strand annealing (SDSA) is the preferred mode of homologous recombination in somatic cells leading to an obligatory non-crossover outcome, thus avoiding the potential for chromosomal rearrangements and loss of heterozygosity. Genetic analysis identified the Srs2 helicase as a prime candidate to promote SDSA. Here, we demonstrate that Srs2 disrupts D-loops in an ATP-dependent fashion and with a distinct polarity. Specifically, we partly reconstitute the SDSA pathway using Rad51, Rad54, RPA, RFC, DNA Polymerase δ with different forms of PCNA. Consistent with genetic data showing the requirement for SUMO and PCNA binding for the SDSA role of Srs2, Srs2 displays a slight but significant preference to disrupt extending D-loops over unextended D-loops when SUMOylated PCNA is present, compared to unmodified PCNA or monoubiquitinated PCNA. Our data establish a biochemical mechanism for the role of Srs2 in crossover suppression by promoting SDSA through disruption of extended D-loops.

Published
2017

23. Colonic Epithelial-Derived Selenoprotein P Is the Source for Antioxidant-Mediated Protection in Colitis-Associated Cancer

Author

Short, Sarah P., Pilat, Jennifer M., Barrett, Caitlyn W., Reddy, Vishruth K., Haberman, Yael, Hendren, Jared R., Marsh, Benjamin J., Keating, Cody E., Motley, Amy K., Hill, Kristina E., Zemper, Anne.E., Washington, M. Kay, Shi, Chanjuan, Chen, Xi, Wilson, Keith T., Hyams, Jeffrey S., Denson, Lee A., Burk, Raymond F., Rosen, Michael J., and Williams, Christopher S.

Published
2021
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25. Dicarbonyl Electrophiles Mediate Inflammation-Induced Gastrointestinal Carcinogenesis

Author

Gobert, Alain P., Boutaud, Olivier, Asim, Mohammad, Zagol-Ikapitte, Irene A., Delgado, Alberto G., Latour, Yvonne L., Finley, Jordan L., Singh, Kshipra, Verriere, Thomas G., Allaman, Margaret M., Barry, Daniel P., McNamara, Kara M., Sierra, Johanna C., Amarnath, Venkataraman, Tantawy, Mohammed N., Bimczok, Diane, Piazuelo, M. Blanca, Washington, M. Kay, Zhao, Shilin, Coburn, Lori A., and Wilson, Keith T.

Published
2021
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27. Purified CDT toxins and a clean deletion within the CDT locus provide novel insights into the contribution of binary toxin in cellular inflammation and Clostridioides difficile infection.

Author

Nabukhotna, Kateryna, Kordus, Shannon L., Shupe, John A., Cano Rodríguez, Rubén, Smith, Anna, Bohannon, Julia K., Washington, M. Kay, and Lacy, D. Borden

Subjects
CLOSTRIDIOIDES difficile, DELETION mutation, INFLAMMASOMES, DENDRITIC cells, ANIMAL culture
Abstract

Clostridioides difficile is a spore-forming pathogen and the most common cause of healthcare-associated diarrhea and colitis in the United States. Besides producing the main virulence factors, toxin A (TcdA) and toxin B (TcdB), many of the common clinical strains encode the C. difficile transferase (CDT) binary toxin. The role of CDT in the context of C. difficile infection (CDI) is poorly understood. Inflammation is a hallmark of CDI and multiple mechanisms of inflammasome activation have been reported for TcdA, TcdB, and the organism. Some studies have suggested that CDT contributes to this inflammation through a TLR2-dependent priming mechanism that leads to the suppression of protective eosinophils. Here, we show that CDT does not prime but instead activates the inflammasome in bone marrow-derived dendritic cells (BMDCs). In bone marrow-derived macrophages (BMDMs), the cell binding and pore-forming component of the toxin, CDTb, alone activates the inflammasome and is dependent on K+ efflux. The activation is not observed in the presence of CDTa and is not observed in BMDMs derived from Nlrp3-/- mice suggesting the involvement of the NLRP3 inflammasome. However, we did not observe evidence of CDT-dependent inflammasome priming or activation in vivo. Mice were infected with R20291 and an isogenic CRISPR/Cas9-generated R20291 ΔcdtB strain of C. difficile. While CDT contributes to increased weight loss and cecal edema at 2 days post infection, the relative levels of inflammasome-associated cytokines, IL-1β and IL-18, in the cecum and distal colon are unchanged. We also saw CDT-dependent weightloss in Nlrp3-/- mice, suggesting that the increased weightloss associated with the presence of CDT is not a result of NLRP3-dependent inflammasome activation. This study highlights the importance of studying gene deletions in the context of otherwise fully isogenic strains and the challenge of translating toxin-specific cellular responses into a physiological context, especially when multiple toxins are acting at the same time. Author summary: Clostridioides difficile is a pathogen causing life-threatening diarrhea. C. difficile transferase (CDT) toxin is present in many strains associated with severe disease but its role during C. difficile infection is unclear. In this study, we show that the pore forming subunit, CDTb, activates the inflammasome in myeloid-derived murine cells. While we found that CDT contributes to weight loss in a C. difficile mouse infection model, this was independent of the inflammasome function. This study highlights the importance of studying gene deletions in the context of otherwise fully isogenic strains and the challenge of translating findings in tissue culture models to animal infections. However, it does reveal an additive role for CDT in the tissue edema that occurs in the murine model of acute infection and is consistent with the idea that CDT contributes to the severity of CDI symptoms. [ABSTRACT FROM AUTHOR]

Published
2024
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28. Succinate Produced by Intestinal Microbes Promotes Specification of Tuft Cells to Suppress Ileal Inflammation

Author

Banerjee, Amrita, Herring, Charles A., Chen, Bob, Kim, Hyeyon, Simmons, Alan J., Southard-Smith, Austin N., Allaman, Margaret M., White, James R., Macedonia, Mary C., Mckinley, Eliot T., Ramirez-Solano, Marisol A., Scoville, Elizabeth A., Liu, Qi, Wilson, Keith T., Coffey, Robert J., Washington, M. Kay, Goettel, Jeremy A., and Lau, Ken S.

Published
2020
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31. A human milk oligosaccharide prevents intestinal inflammation in adulthood via modulating gut microbial metabolism

Author

Schalich, Kasey M., primary, Buendia, Matthew A., additional, Kaur, Harpreet, additional, Choksi, Yash A., additional, Washington, M. Kay, additional, Codreanu, Gabriela S., additional, Sherrod, Stacy D., additional, McLean, John A., additional, Peek, Jr., Richard M., additional, Acra, Sari A., additional, Townsend, Steven D., additional, and Yan, Fang, additional

Published
2024
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32. Biomarkers of NAFLD progression: a lipidomics approach to an epidemic 1 [S]

Author

Gorden, D Lee, Myers, David S, Ivanova, Pavlina T, Fahy, Eoin, Maurya, Mano R, Gupta, Shakti, Min, Jun, Spann, Nathanael J, McDonald, Jeffrey G, Kelly, Samuel L, Duan, Jingjing, Sullards, M Cameron, Leiker, Thomas J, Barkley, Robert M, Quehenberger, Oswald, Armando, Aaron M, Milne, Stephen B, Mathews, Thomas P, Armstrong, Michelle D, Li, Chijun, Melvin, Willie V, Clements, Ronald H, Washington, M Kay, Mendonsa, Alisha M, Witztum, Joseph L, Guan, Ziqiang, Glass, Christopher K, Murphy, Robert C, Dennis, Edward A, Merrill, Alfred H, Russell, David W, Subramaniam, Shankar, and Brown, H Alex

Subjects
Medical Biochemistry and Metabolomics, Biomedical and Clinical Sciences, Chronic Liver Disease and Cirrhosis, Digestive Diseases, Hepatitis, Liver Disease, Clinical Research, Oral and gastrointestinal, Adult, Biomarkers, Double-Blind Method, Female, Humans, Lipids, Male, Middle Aged, Non-alcoholic Fatty Liver Disease, Polymorphism, Single Nucleotide, diagnostic tools, mass spectrometry, phospholipids, sphingolipids, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, Biochemistry and Cell Biology, Biochemistry & Molecular Biology, Biochemistry and cell biology, Medical biochemistry and metabolomics
Abstract

The spectrum of nonalcoholic fatty liver disease (NAFLD) includes steatosis, nonalcoholic steatohepatitis (NASH), and cirrhosis. Recognition and timely diagnosis of these different stages, particularly NASH, is important for both potential reversibility and limitation of complications. Liver biopsy remains the clinical standard for definitive diagnosis. Diagnostic tools minimizing the need for invasive procedures or that add information to histologic data are important in novel management strategies for the growing epidemic of NAFLD. We describe an "omics" approach to detecting a reproducible signature of lipid metabolites, aqueous intracellular metabolites, SNPs, and mRNA transcripts in a double-blinded study of patients with different stages of NAFLD that involves profiling liver biopsies, plasma, and urine samples. Using linear discriminant analysis, a panel of 20 plasma metabolites that includes glycerophospholipids, sphingolipids, sterols, and various aqueous small molecular weight components involved in cellular metabolic pathways, can be used to differentiate between NASH and steatosis. This identification of differential biomolecular signatures has the potential to improve clinical diagnosis and facilitate therapeutic intervention of NAFLD.

Published
2015

34. Distinct roles for interleukin-23 receptor signaling in regulatory T cells in sporadic and inflammation-associated carcinogenesis

Author

Jacobse, Justin, primary, Pilat, Jennifer M., additional, Li, Jing, additional, Brown, Rachel E., additional, Kwag, Aaron, additional, Buendia, Matthew A., additional, Choksi, Yash A., additional, Washington, M. Kay, additional, Williams, Christopher S., additional, Markham, Nicholas O., additional, Short, Sarah P., additional, and Goettel, Jeremy A., additional

Published
2024
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37. BVES is required for maintenance of colonic epithelial integrity in experimental colitis by modifying intestinal permeability

Author

Choksi, Yash A., Reddy, Vishruth K., Singh, Kshipra, Barrett, Caitlyn W., Short, Sarah P., Parang, Bobak, Keating, Cody E., Thompson, Joshua J., Verriere, Thomas G., Brown, Rachel E., Piazuelo, M. Blanca, Bader, David M., Washington, M. Kay, Mittal, Mukul K., Brand, Thomas, Gobert, Alain P., Coburn, Lori A., Wilson, Keith T., and Williams, Christopher S.

Published
2018
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40. Epithelial Smad4 Deletion Up-Regulates Inflammation and Promotes Inflammation-Associated Cancer

Author

Means, Anna L., Freeman, Tanner J., Zhu, Jing, Woodbury, Luke G., Marincola-Smith, Paula, Wu, Chao, Meyer, Anne R., Weaver, Connie J., Padmanabhan, Chandrasekhar, An, Hanbing, Zi, Jinghuan, Wessinger, Bronson C., Chaturvedi, Rupesh, Brown, Tasia D., Deane, Natasha G., Coffey, Robert J., Wilson, Keith T., Smith, J. Joshua, Sawyers, Charles L., Goldenring, James R., Novitskiy, Sergey V., Washington, M. Kay, Shi, Chanjuan, and Beauchamp, R. Daniel

Published
2018
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50. Increased intestinal permeability and downregulation of absorptive ion transporters Nhe3 , Dra , and Sglt1 contribute to diarrhea during Clostridioides difficile infection

Author

Peritore-Galve, F. Christopher, primary, Kaji, Izumi, additional, Smith, Anna, additional, Walker, Lauren M., additional, Shupe, John A., additional, Washington, M. Kay, additional, Algood, Holly M. Scott, additional, Dudeja, Pradeep K., additional, Goldenring, James R., additional, and Lacy, D. Borden, additional

Published
2023
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