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Article ; Online: Correction: Radioprotective potential of melatonin against

Khan, Shahanshah / Adhikari, Jawahar Singh / Rizvi, Moshahid Alam / Chaudhury, Nabo Kumar

2022 Volume 29, Issue 1, Page(s) 91

Language	English
Publishing date	2022-11-02
Publishing country	England
Document type	Published Erratum
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-022-00843-w
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Article ; Online: Quantitative Measurement of Mucolytic Enzymes in Fecal Samples.

Khan, Shahanshah / Zaki, Hasan

Bio-protocol

2021 Volume 11, Issue 6, Page(s) e3956

Abstract: The mucus layer in the gastrointestinal tract covers the apical surface of intestinal epithelial cells, protecting the mucosal tissue from enteric pathogen and commensal microorganisms. The mucus is primarily composed of glycosylated protein called ... ...

Abstract	The mucus layer in the gastrointestinal tract covers the apical surface of intestinal epithelial cells, protecting the mucosal tissue from enteric pathogen and commensal microorganisms. The mucus is primarily composed of glycosylated protein called mucins, which are produced by goblet cells, a type of columnar epithelial cells in the intestinal tract. Defective mucin barrier facilitates infection caused by enteric pathogen and triggers inflammation due to invasion of commensal or opportunistic pathogens into the intestinal epithelial mucosa. Several bacterial species in the gut produce enzymes that are capable of degradation of the mucus. Defective mucin production or increased abundance of mucolytic bacteria are clinically linked to inflammatory bowel disease. Measurement of mucolytic enzymes in the feces, therefore, can be implicated in clinical and experimental research on intestinal disorders. Here, we describe a step-by-step procedure for the measurement of the mucolytic enzyme activity in fecal samples.
Language	English
Publishing date	2021-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.3956
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Article ; Online: Crosstalk between NLRP12 and JNK during Hepatocellular Carcinoma

Shahanshah Khan / Hasan Zaki

International Journal of Molecular Sciences, Vol 21, Iss 2, p

2020 Volume 496

Abstract: Hepatocellular carcinoma (HCC), a leading cause of cancer-related death, is initiated and promoted by chronic inflammation. Inflammatory mediators are transcriptionally regulated by several inflammatory signaling pathways, including nuclear factor kappa ... ...

Abstract	Hepatocellular carcinoma (HCC), a leading cause of cancer-related death, is initiated and promoted by chronic inflammation. Inflammatory mediators are transcriptionally regulated by several inflammatory signaling pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK). cJun N-terminal kinase (JNK), a member of the MAPK family, plays a central role in HCC pathogenesis. Pathogen-associated molecular patterns (PAMPs) activate JNK and other MAPK upon recognition by toll-like receptors (TLRs). Apart from TLRs, PAMPs are sensed by several other pattern recognition receptors, including cytosolic NOD-like receptors (NLRs). In a recent study, we demonstrated that the NLR member NLRP12 plays a critical role in suppressing HCC via negative regulation of the JNK pathway. This article briefly reviews the crosstalk between NLRP12 and JNK that occurs during HCC.
Keywords	jnk ; nlrp12 ; hepatocellular carcinoma ; inflammation ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	571
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Radiomitigation by Melatonin in C57BL/6 Mice: Possible Implications as Adjuvant in Radiotherapy and Chemotherapy.

Tripathi, Akanchha Mani / Khan, Shahanshah / Chaudhury, Nabo Kumar

In vivo (Athens, Greece)

2022 Volume 36, Issue 3, Page(s) 1203–1221

Abstract: Background/aim: Melatonin (N-acetyl-5-methoxytryptamine), a chief secretory molecule of the pineal gland, has multiple properties, and numerous clinical investigations regarding its actions are in progress. This study investigated the radiomitigative ... ...

Abstract	Background/aim: Melatonin (N-acetyl-5-methoxytryptamine), a chief secretory molecule of the pineal gland, has multiple properties, and numerous clinical investigations regarding its actions are in progress. This study investigated the radiomitigative role of melatonin in C57BL/6 mice. Materials and methods: Melatonin (100 mg/kg) was orally administered once daily starting at 1 h on day 1 and subsequently every 24 h until day 7 after whole-body irradiation (WBI) and survival was monitored for 30 days. The bone marrow, spleen, and intestine were studied to evaluate the mitigative potential of melatonin after radiation-induced damage. Results: Melatonin significantly improved the survival upto 60% and 90% after 9 Gy (lethal) and 7.5 Gy (sub-lethal) WBI, respectively. Melatonin alleviated WBI-induced myelosuppression and pancytopenia, and increased white blood cell, red blood cell, platelet, and lymphocyte (CD4 Conclusion: Melatonin mitigates the radiation-induced injury in the gastrointestinal and haematopoietic systems. The observed radiomitigative properties of melatonin can also be useful in the context of adjuvant therapy for cancer and radiotherapy.
MeSH term(s)	Adjuvants, Immunologic ; Animals ; Gamma Rays ; Melatonin/pharmacology ; Mice ; Mice, Inbred C57BL ; Radiation Injuries ; Radiation-Protective Agents/pharmacology ; Whole-Body Irradiation/adverse effects
Chemical Substances	Adjuvants, Immunologic ; Radiation-Protective Agents ; Melatonin (JL5DK93RCL)
Language	English
Publishing date	2022-04-27
Publishing country	Greece
Document type	Journal Article
ZDB-ID	807031-3
ISSN	1791-7549 ; 0258-851X
ISSN (online)	1791-7549
ISSN	0258-851X
DOI	10.21873/invivo.12820
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Correction

Shahanshah Khan / Jawahar Singh Adhikari / Moshahid Alam Rizvi / Nabo Kumar Chaudhury

Journal of Biomedical Science, Vol 29, Iss 1, Pp 1-

Radioprotective potential of melatonin against 60Co γ-ray-induced testicular injury in male C57BL/6 mice

2022 Volume 2

Keywords	Medicine ; R
Language	English
Publishing date	2022-11-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Crosstalk between NLRP12 and JNK during Hepatocellular Carcinoma.

Khan, Shahanshah / Zaki, Hasan

International journal of molecular sciences

2020 Volume 21, Issue 2

Abstract	Hepatocellular carcinoma (HCC), a leading cause of cancer-related death, is initiated and promoted by chronic inflammation. Inflammatory mediators are transcriptionally regulated by several inflammatory signaling pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK). cJun N-terminal kinase (JNK), a member of the MAPK family, plays a central role in HCC pathogenesis. Pathogen-associated molecular patterns (PAMPs) activate JNK and other MAPK upon recognition by toll-like receptors (TLRs). Apart from TLRs, PAMPs are sensed by several other pattern recognition receptors, including cytosolic NOD-like receptors (NLRs). In a recent study, we demonstrated that the NLR member NLRP12 plays a critical role in suppressing HCC via negative regulation of the JNK pathway. This article briefly reviews the crosstalk between NLRP12 and JNK that occurs during HCC.
MeSH term(s)	Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; MAP Kinase Kinase 4/metabolism ; MAP Kinase Signaling System ; Neoplasm Proteins/metabolism
Chemical Substances	Intracellular Signaling Peptides and Proteins ; NLRP12 protein, human ; Neoplasm Proteins ; MAP Kinase Kinase 4 (EC 2.7.12.2)
Language	English
Publishing date	2020-01-13
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/ijms21020496
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Article: SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway.

Khan, Shahanshah / Shafiei, Mahnoush S / Longoria, Christopher / Schoggins, John / Savani, Rashmin C / Zaki, Hasan

bioRxiv : the preprint server for biology

2021

Abstract: Pathogenesis of COVID-19 is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation is poorly understood. Here we investigated direct inflammatory functions of major structural proteins of SARS-CoV- ... ...

Abstract	Pathogenesis of COVID-19 is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation is poorly understood. Here we investigated direct inflammatory functions of major structural proteins of SARS-CoV-2. We observed that spike (S) protein potently induces inflammatory cytokines and chemokines including IL-6, IL-1ß, TNFa, CXCL1, CXCL2, and CCL2, but not IFNs in human and mouse macrophages. No such inflammatory response was observed in response to membrane (M), envelope (E), and neucleocapsid (N) proteins. When stimulated with extracellular S protein, human lung epithelial cells A549 also produce inflammatory cytokines and chemokines. Interestingly, epithelial cells expressing S protein intracellularly are non-inflammatory, but elicit an inflammatory response in macrophages when co-cultured. Biochemical studies revealed that S protein triggers inflammation via activation of the NF-κB pathway in a MyD88-dependent manner. Further, such an activation of the NF-κB pathway is abrogated in Tlr2-deficient macrophages. Consistently, administration of S protein induces IL-6, TNF-a, and IL-1 ß in wild-type, but not Tlr2-deficient mice. Together these data reveal a mechanism for the cytokine storm during SARS-CoV-2 infection and suggest that TLR2 could be a potential therapeutic target for COVID-19.
Language	English
Publishing date	2021-03-17
Publishing country	United States
Document type	Preprint
DOI	10.1101/2021.03.16.435700
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Article ; Online: Monitoring built-up area expansion led by industrial transformation in Delhi using geospatial techniques.

Parveen, Neha / Siddiqui, Lubna / Siddiqui, Masood Ahsan / Sarif, Md Nawaj / Islam, Md Safikul / Khan, Shahanshah / Khanam, Nazreen / Mohibul, Sk / Shariq, Mohammad

Environmental science and pollution research international

2022 Volume 30, Issue 49, Page(s) 106936–106950

Abstract: Historically, industrialization has been a catalyst for built-up expansion generated by economic growth that transforms a landscape. In India, there is a paucity of exploration into how the economic shift transforms the cityscape. Therefore, the ... ...

Abstract	Historically, industrialization has been a catalyst for built-up expansion generated by economic growth that transforms a landscape. In India, there is a paucity of exploration into how the economic shift transforms the cityscape. Therefore, the objective of current research work was to monitor built-up growth induced by industrialization using Landsat datasets and registered industry data. The k-means clustering technique was applied for assessing land use/land cover, Shannon entropy for sprawl, and Pearson for correlation between industrial growth and built-up expansion. The results manifest exponential trend in industrialization with 102-year registered industry record along with increase in built-up density from 0.30 in 1989 to 0.69 by 2019 and in the entire Delhi; it rose from 0.16 to 0.39. Furthermore, Shannon entropy confirmed the sprawl and the strong positive correlation was found among built-up of industrial areas and built-up of Delhi and registered industries. The striking chorological change in industrial as well as city's landscape was observed co-occurring with the dynamics of economic reforms. The outcome of current research could be utilized for the sustainable planning of industrial landscape in Delhi and cities with alike geographical conditions.
MeSH term(s)	Urbanization ; Environmental Monitoring/methods ; Cities ; Geography ; India ; Conservation of Natural Resources
Language	English
Publishing date	2022-09-30
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-022-23221-3
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Article ; Online: SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway.

Khan, Shahanshah / Shafiei, Mahnoush S / Longoria, Christopher / Schoggins, John W / Savani, Rashmin C / Zaki, Hasan

eLife

2021 Volume 10

Abstract: The pathogenesis of COVID-19 is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation is poorly understood. Here, we investigated direct inflammatory functions of major structural proteins of SARS- ...

Abstract	The pathogenesis of COVID-19 is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation is poorly understood. Here, we investigated direct inflammatory functions of major structural proteins of SARS-CoV-2. We observed that spike (S) protein potently induced inflammatory cytokines and chemokines, including IL-6, IL-1β, TNFα, CXCL1, CXCL2, and CCL2, but not IFNs in human and mouse macrophages. No such inflammatory response was observed in response to membrane (M), envelope (E), and nucleocapsid (N) proteins. When stimulated with extracellular S protein, human and mouse lung epithelial cells also produced inflammatory cytokines and chemokines. Interestingly, epithelial cells expressing S protein intracellularly were non-inflammatory, but elicited an inflammatory response in macrophages when co-cultured. Biochemical studies revealed that S protein triggers inflammation via activation of the NF-κB pathway in a MyD88-dependent manner. Further, such an activation of the NF-κB pathway was abrogated in Tlr2-deficient macrophages. Consistently, administration of S protein-induced IL-6, TNF-α, and IL-1β in wild-type, but not Tlr2-deficient mice. Notably, upon recognition of S protein, TLR2 dimerizes with TLR1 or TLR6 to activate the NF-κB pathway. Taken together, these data reveal a mechanism for the cytokine storm during SARS-CoV-2 infection and suggest that TLR2 could be a potential therapeutic target for COVID-19.
MeSH term(s)	A549 Cells ; Animals ; HEK293 Cells ; Humans ; Inflammation/virology ; Mice ; NF-kappa B/physiology ; SARS-CoV-2/physiology ; Signal Transduction ; Spike Glycoprotein, Coronavirus/immunology ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/metabolism
Chemical Substances	NF-kappa B ; Spike Glycoprotein, Coronavirus ; TLR2 protein, human ; Tlr2 protein, mouse ; Toll-Like Receptor 2 ; spike protein, SARS-CoV-2
Language	English
Publishing date	2021-12-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.68563
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Article ; Online: NLRP12 downregulates the Wnt/β-catenin pathway via interaction with STK38 to suppress colorectal cancer

Shahanshah Khan / Youn-Tae Kwak / Lan Peng / Shuiqing Hu / Brandi L. Cantarel / Cheryl M. Lewis / Yunpeng Gao / Ram S. Mani / Thirumala-Devi Kanneganti / Hasan Zaki

The Journal of Clinical Investigation, Vol 133, Iss

2023 Volume 19

Abstract: Colorectal cancer (CRC) at advanced stages is rarely curable, underscoring the importance of exploring the mechanism of CRC progression and invasion. NOD-like receptor family member NLRP12 was shown to suppress colorectal tumorigenesis, but the precise ... ...

Abstract	Colorectal cancer (CRC) at advanced stages is rarely curable, underscoring the importance of exploring the mechanism of CRC progression and invasion. NOD-like receptor family member NLRP12 was shown to suppress colorectal tumorigenesis, but the precise mechanism was unknown. Here, we demonstrate that invasive adenocarcinoma development in Nlrp12-deficient mice is associated with elevated expression of genes involved in proliferation, matrix degradation, and epithelial-mesenchymal transition. Signaling pathway analysis revealed higher activation of the Wnt/β-catenin pathway, but not NF-κB and MAPK pathways, in the Nlrp12-deficient tumors. Using Nlrp12–conditional knockout mice, we revealed that NLRP12 downregulates β-catenin activation in intestinal epithelial cells, thereby suppressing colorectal tumorigenesis. Consistent with this, Nlrp12-deficient intestinal organoids and CRC cells showed increased proliferation, accompanied by higher activation of β-catenin in vitro. With proteomic studies, we identified STK38 as an interacting partner of NLRP12 involved in the inhibition of phosphorylation of GSK3β, leading to the degradation of β-catenin. Consistently, the expression of NLRP12 was significantly reduced, while p-GSK3β and β-catenin were upregulated in mouse and human colorectal tumor tissues. In summary, NLRP12 is a potent negative regulator of the Wnt/β-catenin pathway, and the NLRP12/STK38/GSK3β signaling axis could be a promising therapeutic target for CRC.
Keywords	Gastroenterology ; Medicine ; R
Subject code	570
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	American Society for Clinical Investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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