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Article ; Online: Possible role of IL-23 inhibitor in autoimmune hemolytic anemia.

Premnath, Naveen / Pandey, Urvashi / Pandey, Mohak / Venuprasad, K

2023 Volume 111, Issue 3, Page(s) 506–508

Abstract: Rituximab and prednisone are commonly used treatments for autoimmune hemolytic anemia (AIHA), where the body's immune system attacks and destroys its red blood cells. However, some AIHA patients may become refractory to rituximab treatment, and this can ... ...

Abstract	Rituximab and prednisone are commonly used treatments for autoimmune hemolytic anemia (AIHA), where the body's immune system attacks and destroys its red blood cells. However, some AIHA patients may become refractory to rituximab treatment, and this can result in continued hemolysis and persistent anemia, making it challenging for affected individuals to manage their symptoms. The underlying causes of rituximab refractoriness in AIHA patients can be complex and vary from patient to patient. Herein, we present a case of newly diagnosed warm and cold AIHA that remained in remission with an interleukin-23 inhibitor.
MeSH term(s)	Humans ; Anemia, Hemolytic, Autoimmune/diagnosis ; Anemia, Hemolytic, Autoimmune/drug therapy ; Anemia, Hemolytic, Autoimmune/etiology ; Rituximab/therapeutic use ; Interleukin Inhibitors ; Hemolysis ; Interleukin-23
Chemical Substances	Rituximab (4F4X42SYQ6) ; Interleukin Inhibitors ; Interleukin-23
Language	English
Publishing date	2023-06-06
Publishing country	England
Document type	Case Reports
ZDB-ID	392482-8
ISSN	1600-0609 ; 0902-4441
ISSN (online)	1600-0609
ISSN	0902-4441
DOI	10.1111/ejh.14020
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Article ; Online: NLRP6 in host defense and intestinal inflammation.

Venuprasad, K / Theiss, Arianne L

Cell reports

2021 Volume 35, Issue 4, Page(s) 109043

Abstract: NLRP6 is a member of the NLR (nucleotide-oligomerization domain-like receptor) family of proteins that recognize pathogen-derived factors and damage-associated molecular patterns in the cytosol. The function of NLRP6 has been attributed to the ... ...

Abstract	NLRP6 is a member of the NLR (nucleotide-oligomerization domain-like receptor) family of proteins that recognize pathogen-derived factors and damage-associated molecular patterns in the cytosol. The function of NLRP6 has been attributed to the maintenance of epithelial integrity and host defense against microbial infections. Under some physiological conditions, NLRP6 forms a complex with ASC and caspase-1 or caspase-11 to form an inflammasome complex cleaving pro-interleukin-1β (IL-1β) and IL-18 into their biologically active forms. Here, we summarize recent advances in the understanding of the mechanisms of activation of the NLRP6 inflammasome and discuss its relevance to human disease.
MeSH term(s)	Humans ; Inflammasomes/metabolism ; Inflammation/physiopathology ; Intestinal Mucosa/pathology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
Language	English
Publishing date	2021-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.109043
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Article ; Online: RORγt protein modifications and IL-17-mediated inflammation.

Kumar, Ritesh / Theiss, Arianne L / Venuprasad, K

Trends in immunology

2021 Volume 42, Issue 11, Page(s) 1037–1050

Abstract: RORγt, the master transcription factor for cytokine interleukin (IL)-17, is expressed explicitly in Th17 cells, γδT cells, and type 3 innate lymphoid cells in mice and humans. Since dysregulated IL-17 expression is strongly linked to several human ... ...

Abstract	RORγt, the master transcription factor for cytokine interleukin (IL)-17, is expressed explicitly in Th17 cells, γδT cells, and type 3 innate lymphoid cells in mice and humans. Since dysregulated IL-17 expression is strongly linked to several human inflammatory diseases, the RORγt-IL-17 axis has been the focus of intense research. Recently, several studies have shown that RORγt is modified by multiple post-translational mechanisms, including ubiquitination, acetylation, SUMOylation, and phosphorylation. This review discusses how post-translational modifications modulate RORγt function and its turnover to regulate IL-17-driven inflammation. Broad knowledge of these pathways is crucial for a clear understanding of the pathogenic role of RORγt
MeSH term(s)	Animals ; Cell Differentiation ; Humans ; Immunity, Innate ; Inflammation/metabolism ; Interleukin-17/metabolism ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Protein Processing, Post-Translational ; Th17 Cells
Chemical Substances	Interleukin-17 ; Nuclear Receptor Subfamily 1, Group F, Member 3
Language	English
Publishing date	2021-10-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2021.09.005
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Zs.A 1601: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 2: Show issues

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Article ; Online: Cbl-b and itch: key regulators of peripheral T-cell tolerance.

Venuprasad, K

Cancer research

2010 Volume 70, Issue 8, Page(s) 3009–3012

Abstract: E3 ligases Cbl-b and Itch have emerged as dominant "tolerogenic" regulators of T cells because their deficiency results in severe autoimmune diseases. Cbl-b and Itch ligase activity regulate T-cell anergy and development of Foxp3+ regulatory T cells ( ... ...

Abstract	E3 ligases Cbl-b and Itch have emerged as dominant "tolerogenic" regulators of T cells because their deficiency results in severe autoimmune diseases. Cbl-b and Itch ligase activity regulate T-cell anergy and development of Foxp3+ regulatory T cells (Treg) in the periphery by modulating key components of T-cell receptor (TCR) and transforming growth factor-beta (TGF-beta) signaling. Manipulation of Cbl-b and Itch activities may provide unique opportunities to develop future therapies for immune disorders such as autoimmunity and cancer.
MeSH term(s)	Animals ; Forkhead Transcription Factors/biosynthesis ; Humans ; Immune System ; Immune Tolerance ; Mice ; Neoplasms/metabolism ; Proto-Oncogene Proteins c-cbl/metabolism ; Repressor Proteins/metabolism ; Signal Transduction ; T-Lymphocytes/cytology ; T-Lymphocytes/metabolism ; T-Lymphocytes, Regulatory/cytology ; Transforming Growth Factor beta1/metabolism ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	FOXP3 protein, human ; Forkhead Transcription Factors ; Repressor Proteins ; Transforming Growth Factor beta1 ; ITCH protein, human (EC 2.3.2.26) ; Itch protein, mouse (EC 2.3.2.26) ; Proto-Oncogene Proteins c-cbl (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; CBL protein, human (EC 6.3.2.-) ; Cbl protein, mouse (EC 6.3.2.-)
Language	English
Publishing date	2010-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-09-4076
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Uh III Zs.135/5: Show issues

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Article ; Online: Gut Microbiota Contributes to Spontaneous Colitis in E3 Ligase Itch-Deficient Mice.

Kathania, Mahesh / Tsakem, Elviche L / Theiss, Arianne L / Venuprasad, K

Journal of immunology (Baltimore, Md. : 1950)

2020 Volume 204, Issue 8, Page(s) 2277–2284

Abstract: Inflammatory bowel diseases are associated with complex shifts in microbiota composition. However, it remains unclear whether specific subsets of commensal bacteria induce inflammatory bowel diseases in genetically susceptible hosts. In this study, we ... ...

Abstract	Inflammatory bowel diseases are associated with complex shifts in microbiota composition. However, it remains unclear whether specific subsets of commensal bacteria induce inflammatory bowel diseases in genetically susceptible hosts. In this study, we found that deficiency of the E3 ligase Itch, which leads to spontaneous colitis and rectal prolapse, is associated with alteration of the gut microbiota. 16S rRNA sequencing showed expansion of colitogenic
MeSH term(s)	Animals ; Colitis/microbiology ; Female ; Gastrointestinal Microbiome ; Inflammation/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; RNA, Ribosomal, 16S/genetics ; Ubiquitin-Protein Ligases/deficiency
Chemical Substances	RNA, Ribosomal, 16S ; Itch protein, mouse (EC 2.3.2.26) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2020-03-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1701478
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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Show issues

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Article ; Online: Pak2-mediated phosphorylation promotes RORγt ubiquitination and inhibits colonic inflammation.

Kathania, Mahesh / Kumar, Ritesh / Lenou, Elviche Taskem / Basrur, Venkatesha / Theiss, Arianne L / Chernoff, Jonathan / Venuprasad, K

Cell reports

2022 Volume 40, Issue 11, Page(s) 111345

Abstract: Dysregulated interleukin-17 (IL-17) expression and its downstream signaling is strongly linked to inflammatory bowel diseases (IBDs). However, the molecular mechanisms by which the function of RORγt, the transcription factor of IL-17, is regulated ... ...

Abstract	Dysregulated interleukin-17 (IL-17) expression and its downstream signaling is strongly linked to inflammatory bowel diseases (IBDs). However, the molecular mechanisms by which the function of RORγt, the transcription factor of IL-17, is regulated remains elusive. By a mass spectrometry-based approach, we identify that Pak2, a serine (S)/threonine (T) kinase, directly associates with RORγt. Pak2 recognizes a conserved KRLS motif within RORγt and phosphorylates the S-316 within this motif. Genetic deletion of Pak2 in Th17 cells reduces RORγt phosphorylation, increases IL-17 expression, and induces severe colitis upon adoptive transfer to Rag1
MeSH term(s)	Animals ; Colitis ; Inflammation ; Interleukin-17/metabolism ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Phosphorylation ; Ubiquitination ; p21-Activated Kinases/metabolism
Chemical Substances	Interleukin-17 ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Pak2 protein, mouse (EC 2.7.11.1) ; p21-Activated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-09-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111345
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Article ; Online: Genetic improvement of iron toxicity tolerance in rice-progress, challenges and prospects in West Africa

Sikirou, M. / Saito, Kazuki / Achigan-Dako, E.G. / Drame, K.N. / Ahanchédé, A. / Venuprasad, R.

Plant Production Science

2022

Keywords	rice ; plant breeding ; plant genetics ; iron ; toxicology
Language	English
Publishing date	2022-01-27T15:05:27Z
Publisher	Informa UK Limited
Publishing country	fr
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Transcriptional profiling of the leaves of near-isogenic rice lines with contrasting drought tolerance at the reproductive stage in response to water deficit

Moumeni, A. / Satoh, K. / Venuprasad, R. / Serraj, R. / Kumar, A. / Leung, H. / Kikuchi, S.

BMC Genomics

2022

Keywords	oryza sativa ; rice ; water ; drought ; plant breeding
Language	English
Publishing date	2022-03-03T14:52:57Z
Publisher	Springer
Publishing country	fr
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Inner mitochondrial membrane protein Prohibitin 1 mediates Nix-induced, Parkin-independent mitophagy.

Alula, Kibrom M / Delgado-Deida, Yaritza / Callahan, Rosemary / Till, Andreas / Underwood, Lucia / Thompson, Winston E / Souza, Rhonda F / Dassopoulos, Themistocles / Onyiah, Joseph / Venuprasad, K / Theiss, Arianne L

Scientific reports

2023 Volume 13, Issue 1, Page(s) 18

Abstract: Autophagy of damaged mitochondria, called mitophagy, is an important organelle quality control process involved in the pathogenesis of inflammation, cancer, aging, and age-associated diseases. Many of these disorders are associated with altered ... ...

Abstract	Autophagy of damaged mitochondria, called mitophagy, is an important organelle quality control process involved in the pathogenesis of inflammation, cancer, aging, and age-associated diseases. Many of these disorders are associated with altered expression of the inner mitochondrial membrane (IMM) protein Prohibitin 1. The mechanisms whereby dysfunction occurring internally at the IMM and matrix activate events at the outer mitochondrial membrane (OMM) to induce mitophagy are not fully elucidated. Using the gastrointestinal epithelium as a model system highly susceptible to autophagy inhibition, we reveal a specific role of Prohibitin-induced mitophagy in maintaining intestinal homeostasis. We demonstrate that Prohibitin 1 induces mitophagy in response to increased mitochondrial reactive oxygen species (ROS) through binding to mitophagy receptor Nix/Bnip3L and independently of Parkin. Prohibitin 1 is required for ROS-induced Nix localization to mitochondria and maintaining homeostasis of epithelial cells highly susceptible to mitochondrial dysfunction.
MeSH term(s)	Mitochondrial Membranes/metabolism ; Mitophagy ; Prohibitins ; Reactive Oxygen Species/metabolism ; Mitochondria/metabolism ; Autophagy ; Membrane Proteins/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Mitochondrial Proteins/metabolism
Chemical Substances	Prohibitins ; Reactive Oxygen Species ; Membrane Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Mitochondrial Proteins
Language	English
Publishing date	2023-01-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-26775-x
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Article ; Online: RORγt-Raftlin1 complex regulates the pathogenicity of Th17 cells and colonic inflammation.

Singh, Amir Kumar / Kumar, Ritesh / Yin, Jianyi / Brooks Ii, John F / Kathania, Mahesh / Mukherjee, Sandip / Kumar, Jitendra / Conlon, Kevin P / Basrur, Venkatesha / Chen, Zhe / Han, Xianlin / Hooper, Lora V / Burstein, Ezra / Venuprasad, K

Nature communications

2023 Volume 14, Issue 1, Page(s) 4972

Abstract: Th17 cells that produce Interleukin IL-17 are pathogenic in many human diseases, including inflammatory bowel disease, but are, paradoxically, essential for maintaining the integrity of the intestinal barrier in a non-inflammatory state. However, the ... ...

Abstract	Th17 cells that produce Interleukin IL-17 are pathogenic in many human diseases, including inflammatory bowel disease, but are, paradoxically, essential for maintaining the integrity of the intestinal barrier in a non-inflammatory state. However, the intracellular mechanisms that regulate distinct transcriptional profiles and functional diversity of Th17 cells remain unclear. Here we show Raftlin1, a lipid raft protein, specifically upregulates and forms a complex with RORγt in pathogenic Th17 cells. Disruption of the RORγt-Raftlin1 complex results in the reduction of pathogenic Th17 cells in response to Citrobacter rodentium; however, there is no effect on nonpathogenic Th17 cells in response to commensal segmented filamentous bacteria. Mechanistically, we show that Raftlin1 recruits distinct phospholipids to RORγt and promotes the pathogenicity of Th17 cells. Thus, we have identified a mechanism that drives the pathogenic function of Th17 cells, which could provide a platform for advanced therapeutic strategies to dampen Th17-mediated inflammatory diseases.
MeSH term(s)	Humans ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics ; Virulence ; Th17 Cells ; Inflammation ; Colon
Chemical Substances	Nuclear Receptor Subfamily 1, Group F, Member 3
Language	English
Publishing date	2023-08-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-40622-1
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