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Article ; Online: Microbial influences on severity and sex bias of systemic autoimmunity.

Lee, Jean / Reiman, Derek / Singh, Samara / Chang, Anthony / Morel, Laurence / Chervonsky, Alexander V

2024

Abstract: Commensal microbes have the capacity to affect development and severity of autoimmune diseases. Germ-free (GF) animals have proven to be a fine tool to obtain definitive answers to the queries about the microbial role in these diseases. Moreover, GF and ... ...

Abstract	Commensal microbes have the capacity to affect development and severity of autoimmune diseases. Germ-free (GF) animals have proven to be a fine tool to obtain definitive answers to the queries about the microbial role in these diseases. Moreover, GF and gnotobiotic animals can be used to dissect the complex symptoms and determine which are regulated (enhanced or attenuated) by microbes. These include disease manifestations that are sex biased. Here, we review comparative analyses conducted between GF and Specific-Pathogen Free (SPF) mouse models of autoimmunity. We present data from the B6;NZM-Sle1
Language	English
Publishing date	2024-05-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13341
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Article: Emerging Role of CREB in Epithelial to Mesenchymal Plasticity of Pancreatic Cancer.

Mehra, Siddharth / Singh, Samara / Nagathihalli, Nagaraj

Frontiers in oncology

2022 Volume 12, Page(s) 925687

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive solid malignancy with a high rate of metastasis and therapeutic resistance as its major hallmarks. Although a defining mutational event in pancreatic cancer initiation is the presence of ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is an aggressive solid malignancy with a high rate of metastasis and therapeutic resistance as its major hallmarks. Although a defining mutational event in pancreatic cancer initiation is the presence of oncogenic
Language	English
Publishing date	2022-06-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.925687
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Article ; Online: Overcoming Acquired Drug Resistance to Cancer Therapies through Targeted STAT3 Inhibition.

Singh, Sunanda / Gomez, Hector J / Thakkar, Shreya / Singh, Samara P / Parihar, Ashutosh S

International journal of molecular sciences

2023 Volume 24, Issue 5

Abstract: Anti-neoplastic agents for cancer treatment utilize many different mechanisms of action and, when combined, can result in potent inhibition of cancer growth. Combination therapies can result in long-term, durable remission or even cure; however, too many ...

Abstract	Anti-neoplastic agents for cancer treatment utilize many different mechanisms of action and, when combined, can result in potent inhibition of cancer growth. Combination therapies can result in long-term, durable remission or even cure; however, too many times, these anti-neoplastic agents lose their efficacy due to the development of acquired drug resistance (ADR). In this review, we evaluate the scientific and medical literature that elucidate STAT3-mediated mechanisms of resistance to cancer therapeutics. Herein, we have found that at least 24 different anti-neoplastic agents-standard toxic chemotherapeutic agents, targeted kinase inhibitors, anti-hormonal agents, and monoclonal antibodies-that utilize the STAT3 signaling pathway as one mechanism of developing therapeutic resistance. Targeting STAT3, in combination with existing anti-neoplastic agents, may prove to be a successful therapeutic strategy to either prevent or even overcome ADR to standard and novel cancer therapies.
MeSH term(s)	Humans ; Antibodies, Monoclonal/pharmacology ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Drug Resistance, Neoplasm/drug effects ; Neoplasms/drug therapy ; Signal Transduction ; STAT3 Transcription Factor/antagonists & inhibitors
Chemical Substances	Antibodies, Monoclonal ; Antineoplastic Agents ; STAT3 protein, human ; STAT3 Transcription Factor
Language	English
Publishing date	2023-03-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24054722
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Article ; Online: Interleukin-1 signaling in solid organ malignancies.

Dosch, Austin R / Singh, Samara / Nagathihalli, Nagaraj S / Datta, Jashodeep / Merchant, Nipun B

Biochimica et biophysica acta. Reviews on cancer

2021 Volume 1877, Issue 1, Page(s) 188670

Abstract: As inflammation plays a critical role in the development and progression of cancer, therapeutic targeting of cytokine pathways involved in both tumorigenesis and dictating response to clinical treatments are of significant interest. Recent evidence has ... ...

Abstract	As inflammation plays a critical role in the development and progression of cancer, therapeutic targeting of cytokine pathways involved in both tumorigenesis and dictating response to clinical treatments are of significant interest. Recent evidence has highlighted the importance of the pro-inflammatory cytokine interleukin-1 (IL-1) as a key mediator of tumor growth, metastatic disease spread, immunosuppression, and drug resistance in cancer. IL-1 promotes tumorigenesis through diverse mechanisms, including the activation of oncogenic signaling pathways directly in tumor cells and via orchestrating crosstalk between the cellular constituents of the tumor microenvironment (TME), thereby driving cancer growth. This review will provide an overview of IL-1 signaling and physiology and summarize the disparate mechanisms involving IL-1 in tumorigenesis and cancer progression. Additionally, clinical studies targeting IL-1 signaling in the management of solid organ tumors will be summarized herein.
MeSH term(s)	Carcinogenesis ; Humans ; Interleukin-1 ; Neoplasms/pathology ; Signal Transduction/physiology ; Tumor Microenvironment
Chemical Substances	Interleukin-1
Language	English
Publishing date	2021-12-16
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2918802-7
ISSN	1879-2561 ; 0304-419X
ISSN (online)	1879-2561
ISSN	0304-419X
DOI	10.1016/j.bbcan.2021.188670
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Article ; Online: A Broad-Based Characterization of a Cell-Penetrating, Single Domain Camelid Bi-Specific Antibody Monomer That Targets STAT3 and KRAS Dependent Cancers.

Singh, Sunanda / Murillo, Genoveva / Richner, Justin / Singh, Samara P / Berleth, Erica / Kumar, Vijay / Mehta, Rajendra / Ramiya, Vijay / Parihar, Ashutosh S

International journal of molecular sciences

2022 Volume 23, Issue 14

Abstract: STAT3 and KRAS regulate cell proliferation, survival, apoptosis, cell migration, and angiogenesis. Aberrant expression of STAT3 and mutant active forms of KRAS have been well-established in the induction and maintenance of multiple cancers. STAT3 and ... ...

Abstract	STAT3 and KRAS regulate cell proliferation, survival, apoptosis, cell migration, and angiogenesis. Aberrant expression of STAT3 and mutant active forms of KRAS have been well-established in the induction and maintenance of multiple cancers. STAT3 and KRAS mutant proteins have been considered anti-cancer targets; however, they are also considered to be clinically "undruggable" intracellular molecules, except for KRAS(G12C). Here we report a first-in-class molecule, a novel, single domain camelid VHH antibody (15 kDa), SBT-100, that binds to both STAT3 and KRAS and can penetrate the tumor cell membrane, and significantly inhibit cancer cell growth. Additionally, SBT-100 inhibits KRAS GTPase activity and downstream phosphorylation of ERK in vitro. In addition, SBT-100 inhibits the growth of multiple human cancers in vitro and in vivo. These results demonstrate the feasibility of targeting hard-to-reach aberrant intracellular transcription factors and signaling proteins simultaneously with one VHH to improve cancer therapies.
MeSH term(s)	Antibodies, Bispecific/pharmacology ; Antineoplastic Agents, Immunological ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Mutation ; Neoplasms/immunology ; Neoplasms/therapy ; Proto-Oncogene Proteins p21(ras)/genetics ; STAT3 Transcription Factor ; Single-Domain Antibodies/pharmacology
Chemical Substances	Antibodies, Bispecific ; Antineoplastic Agents, Immunological ; KRAS protein, human ; STAT3 Transcription Factor ; STAT3 protein, human ; Single-Domain Antibodies ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2022-07-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23147565
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Article ; Online: Tumor Cell-Intrinsic p38 MAPK Signaling Promotes IL1α-Mediated Stromal Inflammation and Therapeutic Resistance in Pancreatic Cancer.

Singh, Samara P / Dosch, Austin R / Mehra, Siddharth / De Castro Silva, Iago / Bianchi, Anna / Garrido, Vanessa T / Zhou, Zhiqun / Adams, Andrew / Amirian, Haleh / Box, Edmond W / Sun, Xiaodian / Ban, Yuguang / Datta, Jashodeep / Nagathihalli, Nagaraj S / Merchant, Nipun B

Cancer research

2024 Volume 84, Issue 8, Page(s) 1320–1332

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is characterized by a KRAS-driven inflammatory program and a desmoplastic stroma, which contribute to the profoundly chemoresistant phenotype. The tumor stroma contains an abundance of cancer-associated fibroblasts ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is characterized by a KRAS-driven inflammatory program and a desmoplastic stroma, which contribute to the profoundly chemoresistant phenotype. The tumor stroma contains an abundance of cancer-associated fibroblasts (CAF), which engage in extensive paracrine cross-talk with tumor cells to perpetuate protumorigenic inflammation. IL1α, a pleiotropic, tumor cell-derived cytokine, plays a critical role in shaping the stromal landscape. To provide insights into the molecular mechanisms regulating IL1A expression in PDAC, we performed transcriptional profiling of The Cancer Genome Atlas datasets and pharmacologic screening in PDAC cells and identified p38α MAPK as a key positive regulator of IL1A expression. Both genetic and pharmacologic inhibition of p38 MAPK significantly diminished IL1α production in vitro. Chromatin- and coimmunoprecipitation analyses revealed that p38 MAPK coordinates the transcription factors Sp1 and the p65 subunit of NFκB to drive IL1A overexpression. Single-cell RNA sequencing of a highly desmoplastic murine PDAC model, Ptf1aCre/+; LSL-KrasG12D/+; Tgfbr2flox/flox (PKT), confirmed that p38 MAPK inhibition significantly decreases tumor cell-derived Il1a and attenuates the inflammatory CAF phenotype in a paracrine IL1α-dependent manner. Furthermore, p38 MAPK inhibition favorably modulated intratumoral immunosuppressive myeloid populations and augmented chemotherapeutic efficacy to substantially reduce tumor burden and improve overall survival in PKT mice. These findings illustrate a cellular mechanism of tumor cell-intrinsic p38-p65/Sp1-IL1α signaling that is responsible for sustaining stromal inflammation and CAF activation, offering an attractive therapeutic approach to enhance chemosensitivity in PDAC. Significance: Inhibition of p38 MAPK suppresses tumor cell-derived IL1α and attenuates the inflammatory stroma and immunosuppressive tumor microenvironment to overcome chemotherapeutic resistance in pancreatic cancer.
MeSH term(s)	Mice ; Animals ; Drug Resistance, Neoplasm/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Cancer-Associated Fibroblasts/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism ; Inflammation/pathology ; Tumor Microenvironment
Chemical Substances	p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2024-01-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-23-1200
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Article ; Online: Remodeling of Stromal Immune Microenvironment by Urolithin A Improves Survival with Immune Checkpoint Blockade in Pancreatic Cancer.

Mehra, Siddharth / Garrido, Vanessa T / Dosch, Austin R / Lamichhane, Purushottam / Srinivasan, Supriya / Singh, Samara P / Zhou, Zhiqun / De Castro Silva, Iago / Joshi, Chandrashekar / Ban, Yuguang / Datta, Jashodeep / Gilboa, Eli / Merchant, Nipun B / Nagathihalli, Nagaraj S

Cancer research communications

2023 Volume 3, Issue 7, Page(s) 1224–1236

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a significant contributor to cancer-related morbidity and mortality, and it is known for its resistance to conventional treatment regimens, including chemotherapy and immune checkpoint blockade (ICB)-based ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is a significant contributor to cancer-related morbidity and mortality, and it is known for its resistance to conventional treatment regimens, including chemotherapy and immune checkpoint blockade (ICB)-based therapies. We have previously shown that Urolithin A (Uro A), a gut microbial metabolite derived from pomegranates, can target and inhibit Significance: Immunotherapeutic agents are ineffective against pancreatic cancer, mainly due to the immunosuppressive tumor microenvironment and stromal desmoplasia. Our current study demonstrates the therapeutic utility of a novel gut microbial metabolite, Uro A, to remodel the stromal-immune microenvironment and improve overall survival with anti-PD-1 therapy in pancreatic cancer.
MeSH term(s)	Mice ; Animals ; Immune Checkpoint Inhibitors/pharmacology ; CD8-Positive T-Lymphocytes/metabolism ; Phosphatidylinositol 3-Kinases/pharmacology ; Pancreatic Neoplasms/drug therapy ; Carcinoma, Pancreatic Ductal/drug therapy ; Tumor Microenvironment
Chemical Substances	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one (1143-70-0) ; Immune Checkpoint Inhibitors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2023-07-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-22-0329
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Article ; Online: Combined MEK and STAT3 Inhibition Uncovers Stromal Plasticity by Enriching for Cancer-Associated Fibroblasts With Mesenchymal Stem Cell-Like Features to Overcome Immunotherapy Resistance in Pancreatic Cancer.

Datta, Jashodeep / Dai, Xizi / Bianchi, Anna / De Castro Silva, Iago / Mehra, Siddharth / Garrido, Vanessa T / Lamichhane, Purushottam / Singh, Samara P / Zhou, Zhiqun / Dosch, Austin R / Messaggio, Fanuel / Ban, Yuguang / Umland, Oliver / Hosein, Peter J / Nagathihalli, Nagaraj S / Merchant, Nipun B

Gastroenterology

2022 Volume 163, Issue 6, Page(s) 1593–1612

Abstract: Background & aims: We have shown that reciprocally activated rat sarcoma (RAS)/mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) and Janus kinase/signal transducer and activator of transcription 3 (STAT3) pathways mediate ... ...

Abstract	Background & aims: We have shown that reciprocally activated rat sarcoma (RAS)/mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) and Janus kinase/signal transducer and activator of transcription 3 (STAT3) pathways mediate therapeutic resistance in pancreatic ductal adenocarcinoma (PDAC), while combined MEK and STAT3 inhibition (MEKi+STAT3i) overcomes such resistance and alters stromal architecture. We now determine whether MEKi+STAT3i reprograms the cancer-associated fibroblast (CAF) and immune microenvironment to overcome resistance to immune checkpoint inhibition in PDAC. Methods: CAF and immune cell transcriptomes in MEKi (trametinib)+STAT3i (ruxolitinib)-treated vs vehicle-treated Ptf1a Results: MEKi+STAT3i attenuates Il6/Cxcl1-expressing proinflammatory and Lrrc15-expressing myofibroblastic CAF phenotypes while enriching for Ly6a/Cd34-expressing CAFs exhibiting mesenchymal stem cell-like features via scRNAseq in PKT mice. This CAF plasticity is associated with M2-to-M1 reprogramming of tumor-associated macrophages, and enhanced trafficking of cluster of differentiation 8 Conclusions: Combined MEKi+STAT3i mitigates stromal inflammation and enriches for CAF phenotypes with mesenchymal stem cell-like properties to overcome immunotherapy resistance in PDAC.
MeSH term(s)	Mice ; Animals ; Cancer-Associated Fibroblasts ; STAT3 Transcription Factor/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Immunotherapy ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Immunologic Factors ; Mesenchymal Stem Cells ; Adenocarcinoma ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Tumor Microenvironment ; Pancreatic Neoplasms
Chemical Substances	ruxolitinib (82S8X8XX8H) ; STAT3 Transcription Factor ; Immunologic Factors ; Immune Checkpoint Inhibitors
Language	English
Publishing date	2022-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2022.07.076
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Article ; Online: Targeting Tumor-Stromal IL6/STAT3 Signaling through IL1 Receptor Inhibition in Pancreatic Cancer.

Dosch, Austin R / Singh, Samara / Dai, Xizi / Mehra, Siddharth / Silva, Iago De Castro / Bianchi, Anna / Srinivasan, Supriya / Gao, Zhen / Ban, Yuguang / Chen, Xi / Banerjee, Sulagna / Nagathihalli, Nagaraj S / Datta, Jashodeep / Merchant, Nipun B

Molecular cancer therapeutics

2021 Volume 20, Issue 11, Page(s) 2280–2290

Abstract: A hallmark of pancreatic ductal adenocarcinoma (PDAC) is the presence of a dense, desmoplastic stroma and the consequent altered interactions between cancer cells and their surrounding tumor microenvironment (TME) that promote disease progression, ... ...

Abstract	A hallmark of pancreatic ductal adenocarcinoma (PDAC) is the presence of a dense, desmoplastic stroma and the consequent altered interactions between cancer cells and their surrounding tumor microenvironment (TME) that promote disease progression, metastasis, and chemoresistance. We have previously shown that IL6 secreted from pancreatic stellate cells (PSC) stimulates the activation of STAT3 signaling in tumor cells, an established mechanism of therapeutic resistance in PDAC. We have now identified the tumor cell-derived cytokine IL1α as an upstream mediator of IL6 release from PSCs that is involved in STAT3 activation within the TME. Herein, we show that IL1α is overexpressed in both murine and human PDAC tumors and engages with its cognate receptor IL1R1, which is strongly expressed on stromal cells. Further, we show that IL1R1 inhibition using anakinra (recombinant IL1 receptor antagonist) significantly reduces stromal-derived IL6, thereby suppressing IL6-dependent STAT3 activation in human PDAC cell lines. Anakinra treatment results in significant reduction in IL6 and activated STAT3 levels in pancreatic tumors from
MeSH term(s)	Animals ; Humans ; Interleukin-6/metabolism ; Mice ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Receptors, Interleukin-1/antagonists & inhibitors ; Signal Transduction
Chemical Substances	Interleukin-6 ; Receptors, Interleukin-1
Language	English
Publishing date	2021-09-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-21-0083
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Article ; Online: Urolithin A attenuates severity of chronic pancreatitis associated with continued alcohol intake by inhibiting PI3K/AKT/mTOR signaling.

Mehra, Siddharth / Srinivasan, Supriya / Singh, Samara / Zhou, Zhiqun / Garrido, Vanessa / Silva, Iago De Castro / Totiger, Tulasigeri M / Dosch, Austin R / Dai, Xizi / Dawra, Rajinder K / Jala, Venkatakrishna Rao / Shi, Chanjuan / Datta, Jashodeep / VanSaun, Michael / Merchant, Nipun / Nagathihalli, Nagaraj

American journal of physiology. Gastrointestinal and liver physiology

2022 Volume 323, Issue 4, Page(s) G375–G386

Abstract: Heavy alcohol consumption is the dominant risk factor for chronic pancreatitis (CP); however, treatment and prevention strategies for alcoholic chronic pancreatitis (ACP) remains limited. The present study demonstrates that ACP induction in C57BL/6 mice ... ...

Abstract	Heavy alcohol consumption is the dominant risk factor for chronic pancreatitis (CP); however, treatment and prevention strategies for alcoholic chronic pancreatitis (ACP) remains limited. The present study demonstrates that ACP induction in C57BL/6 mice causes significant acinar cell injury, pancreatic stellate cell (PSC) activation, exocrine function insufficiency, and an increased fibroinflammatory response when compared with alcohol or CP alone. Although the withdrawal of alcohol during ACP recovery led to reversion of pancreatic damage, continued alcohol consumption with established ACP perpetuated pancreatic injury. In addition, phosphokinase array and Western blot analysis of ACP-induced mice pancreata revealed activation of the phosphatidylinositol 3 kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) and cyclic AMP response element binding protein (CREB) signaling pathways possibly orchestrating the fibroinflammatory program of ACP pathogenesis. Mice treated with urolithin A (Uro A, a gut-derived microbial metabolite) in the setting of ACP with continued alcohol intake (during the recovery period) showed suppression of AKT and P70S6K activation, and acinar damage was significantly reduced with a parallel reduction in pancreas-infiltrating macrophages and proinflammatory cytokine accumulation. These results collectively provide mechanistic insight into the impact of Uro A on attenuation of ACP severity through suppression of PI3K/AKT/mTOR signaling pathways and can be a useful therapeutic approach in patients with ACP with continuous alcohol intake.
MeSH term(s)	Mice ; Animals ; Proto-Oncogene Proteins c-akt/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Ribosomal Protein S6 Kinases, 70-kDa/metabolism ; Ribosomal Protein S6 Kinases, 70-kDa/pharmacology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Mice, Inbred C57BL ; TOR Serine-Threonine Kinases/metabolism ; Signal Transduction ; Pancreatitis, Alcoholic/pathology ; Sirolimus/pharmacology ; Cytokines/pharmacology ; Alcohol Drinking ; Mammals/metabolism
Chemical Substances	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one (1143-70-0) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; Cyclic AMP Response Element-Binding Protein ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Sirolimus (W36ZG6FT64) ; Cytokines
Language	English
Publishing date	2022-09-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00159.2022
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