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Article ; Online: Oncogenes calling on a lysosomal Ca

Schwartz, Daniella M / Muallem, Shmuel

2019 Volume 20, Issue 4

MeSH term(s)	Calcium Signaling ; Lysosomes ; Oncogenes
Language	English
Publishing date	2019-03-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.15252/embr.201947953
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Article ; Online: Allergic Aspects of IgG4-Related Disease: Implications for Pathogenesis and Therapy.

Michailidou, Despina / Schwartz, Daniella Muallem / Mustelin, Tomas / Hughes, Grant C

Frontiers in immunology

2021 Volume 12, Page(s) 693192

Abstract: IgG4-related disease (IgG4-RD) is a rare systemic fibroinflammatory disease frequently associated with allergy. The pathogenesis of IgG4-RD is poorly understood, and effective therapies are limited. However, IgG4-RD appears to involve some of the same ... ...

Abstract	IgG4-related disease (IgG4-RD) is a rare systemic fibroinflammatory disease frequently associated with allergy. The pathogenesis of IgG4-RD is poorly understood, and effective therapies are limited. However, IgG4-RD appears to involve some of the same pathogenic mechanisms observed in allergic disease, such as T helper 2 (Th2) and regulatory T cell (Treg) activation, IgG4 and IgE hypersecretion, and blood/tissue eosinophilia. In addition, IgG4-RD tissue fibrosis appears to involve activation of basophils and mast cells and their release of alarmins and cytokines. In this article, we review allergy-like features of IgG4-RD and highlight targeted therapies for allergy that have potential in treating patients with IgG4-RD.
MeSH term(s)	Alarmins/metabolism ; Animals ; Cytokines/metabolism ; Fibrosis ; Humans ; Hypersensitivity/immunology ; Hypersensitivity/metabolism ; Hypersensitivity/physiopathology ; Immune System/immunology ; Immune System/metabolism ; Immune System/physiopathology ; Immunoglobulin E/metabolism ; Immunoglobulin G/immunology ; Immunoglobulin G/metabolism ; Immunoglobulin G4-Related Disease/immunology ; Immunoglobulin G4-Related Disease/metabolism ; Immunoglobulin G4-Related Disease/physiopathology ; Signal Transduction
Chemical Substances	Alarmins ; Cytokines ; Immunoglobulin G ; Immunoglobulin E (37341-29-0)
Language	English
Publishing date	2021-07-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.693192
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Article: Social Determinants modulate NK cell activity via obesity, LDL, and DUSP1 signaling.

Baumer, Yvonne / Singh, Komudi / Baez, Andrew S / Gutierrez-Huerta, Christian A / Chen, Long / Igboko, Muna / Turner, Briana S / Yeboah, Josette A / Reger, Robert N / Ortiz-Whittingham, Lola R / Bleck, Christopher K E / Mitchell, Valerie M / Collins, Billy S / Pirooznia, Mehdi / Dagur, Pradeep K / Allan, David S J / Muallem-Schwartz, Daniella / Childs, Richard W / Powell-Wiley, Tiffany M

bioRxiv : the preprint server for biology

2023

Abstract: Adverse social determinants of health (aSDoH) are associated with obesity and related comorbidities like diabetes, cardiovascular disease, and cancer. Obesity is also associated with natural killer cell (NK) dysregulation, suggesting a potential ... ...

Abstract	Adverse social determinants of health (aSDoH) are associated with obesity and related comorbidities like diabetes, cardiovascular disease, and cancer. Obesity is also associated with natural killer cell (NK) dysregulation, suggesting a potential mechanistic link. Therefore, we measured NK phenotypes and function in a cohort of African-American (AA) women from resource-limited neighborhoods. Obesity was associated with reduced NK cytotoxicity and a shift towards a regulatory phenotype.
Language	English
Publishing date	2023-09-15
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.12.556825
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Article ; Online: T Cells in Autoimmunity-Associated Cardiovascular Diseases.

Schwartz, Daniella Muallem / Burma, Aarohan M / Kitakule, Moses M / Luo, Yiming / Mehta, Nehal N

Frontiers in immunology

2020 Volume 11, Page(s) 588776

Abstract: T cells are indisputably critical mediators of atherosclerotic cardiovascular disease (CVD), where they secrete pro-inflammatory cytokines that promote vascular pathology. Equally well-established is the fact that autoimmune diseases, which are mediated ... ...

Abstract	T cells are indisputably critical mediators of atherosclerotic cardiovascular disease (CVD), where they secrete pro-inflammatory cytokines that promote vascular pathology. Equally well-established is the fact that autoimmune diseases, which are mediated by autoreactive T cells, substantially increase the risk of developing CVD. Indeed, as immunomodulatory treatments have become more effective at treating end-organ pathology, CVD has become a leading cause of death in patients with autoimmune diseases. Despite this, investigators have only recently begun to probe the mechanisms by which autoreactive T cells promote CVD in the context of autoimmune diseases. T cells are best-studied in the pathogenesis of systemic vasculitides, where they react to self-antigen in the vessel wall. However, newer studies indicate that T cells also contribute to the increased CVD risk associated with lupus and rheumatoid arthritis. Given the central role of T-cell-derived cytokines in the pathogenesis of psoriasis, the role of these factors in psoriatic CVD is also under investigation. In the future, T cells are likely to represent major targets for the prevention and treatment of CVD in patients with autoimmune diseases.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmunity ; Cardiovascular Diseases/immunology ; Humans ; T-Lymphocytes/immunology
Language	English
Publishing date	2020-10-07
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.588776
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Article ; Online: Ca

Son, Aran / Ahuja, Malini / Schwartz, Daniella M / Varga, Arpad / Swaim, William / Kang, Namju / Maleth, Jozsef / Shin, Dong Min / Muallem, Shmuel

Gastroenterology

2019 Volume 157, Issue 6, Page(s) 1660–1672.e2

Abstract: Background & aims: Pancreatitis is characterized by increased influx of Ca: Methods: We generated mice that expressed SARAF tagged with hemagglutinin, using CRISPR/Cas9 gene editing, and isolated acinar cells. We also performed studies with Saraf: ... ...

Abstract	Background & aims: Pancreatitis is characterized by increased influx of Ca Methods: We generated mice that expressed SARAF tagged with hemagglutinin, using CRISPR/Cas9 gene editing, and isolated acinar cells. We also performed studies with Saraf Results: Pancreatic levels of Ca Conclusions: In mice with pancreatitis, SARAF initially increases but is then degraded, resulting in excessive, pathological Ca
MeSH term(s)	Acinar Cells/pathology ; Animals ; Calcium/metabolism ; Ceruletide/toxicity ; Disease Models, Animal ; HEK293 Cells ; Humans ; Intracellular Calcium-Sensing Proteins/genetics ; Intracellular Calcium-Sensing Proteins/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Neoplasm Proteins/metabolism ; Pancreas/cytology ; Pancreas/pathology ; Pancreatitis/blood ; Pancreatitis/chemically induced ; Pancreatitis/pathology ; Severity of Illness Index ; Stromal Interaction Molecule 1/metabolism
Chemical Substances	Intracellular Calcium-Sensing Proteins ; Membrane Proteins ; Neoplasm Proteins ; SARAF protein, human ; STIM1 protein, human ; Stromal Interaction Molecule 1 ; Ceruletide (888Y08971B) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-09-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; 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.2019.08.042
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Article ; Online: Review. ATP hydrolysis-driven gating in cystic fibrosis transmembrane conductance regulator.

Muallem, Daniella / Vergani, Paola

Philosophical transactions of the Royal Society of London. Series B, Biological sciences

2009 Volume 364, Issue 1514, Page(s) 247–255

Abstract: Proteins belonging to the ATP-binding cassette superfamily couple ATP binding and hydrolysis at conserved nucleotide-binding domains (NBDs) to diverse cellular functions. Most superfamily members are transporters, while cystic fibrosis transmembrane ... ...

Abstract	Proteins belonging to the ATP-binding cassette superfamily couple ATP binding and hydrolysis at conserved nucleotide-binding domains (NBDs) to diverse cellular functions. Most superfamily members are transporters, while cystic fibrosis transmembrane conductance regulator (CFTR), alone, is an ion channel. Despite this functional difference, recent results have suggested that CFTR shares a common molecular mechanism with other members. ATP binds to partial binding sites on the surface of the two NBDs, which then associate to form a NBD dimer, with complete composite catalytic sites now buried at the interface. ATP hydrolysis and gamma-phosphate dissociation, with the loss of molecular contacts linking the two sides of the composite site, trigger dimer dissociation. The conformational signals generated by NBD dimer formation and dissociation are transmitted to the transmembrane domains where, in transporters, they drive the cycle of conformational changes that translocate the substrate across the membrane; in CFTR, they result in opening and closing (gating) of the ion-permeation pathway.
MeSH term(s)	Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/chemistry ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Hydrolysis ; Ion Channel Gating/physiology ; Protein Structure, Tertiary
Chemical Substances	Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Adenosine Triphosphate (8L70Q75FXE) ; Adenosine Triphosphatases (EC 3.6.1.-)
Language	English
Publishing date	2009-01-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208382-6
ISSN	1471-2970 ; 0080-4622 ; 0264-3839 ; 0962-8436
ISSN (online)	1471-2970
ISSN	0080-4622 ; 0264-3839 ; 0962-8436
DOI	10.1098/rstb.2008.0191
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Article: An anion antiporter model of prestin, the outer hair cell motor protein.

Muallem, Daniella / Ashmore, Jonathan

Biophysical journal

2006 Volume 90, Issue 11, Page(s) 4035–4045

Abstract: Cochlear amplification in mammalian hearing relies on an active mechanical feedback process generated by outer hair cells, driven by a protein, prestin (SLC26A5), in the lateral membrane. We have used kinetic models to understand the mechanism by which ... ...

Abstract	Cochlear amplification in mammalian hearing relies on an active mechanical feedback process generated by outer hair cells, driven by a protein, prestin (SLC26A5), in the lateral membrane. We have used kinetic models to understand the mechanism by which prestin might function. We show that the two previous hypotheses of prestin, which assume prestin cannot operate as a transporter, are insufficient to explain previously published data. We propose an alternative model of prestin as an electrogenic anion exchanger, exchanging one Cl(-) ion for one divalent or two monovalent anions. This model can reproduce the key aspects of previous experimental observations. The experimentally observed charge movements are produced by the translocation of one Cl(-) ion combined with intrinsic positively charged residues, while the transport of the counteranion is electroneutral. We tested the model with measurements of the Cl(-) dependence of charge movement, using SO(4)(2-) to replace Cl(-). The data was compatible with the predictions of the model, suggesting that prestin does indeed function as a transporter.
MeSH term(s)	Animals ; Anions/metabolism ; Antiporters/physiology ; Chlorides/metabolism ; Electric Conductivity ; Guinea Pigs ; Hair Cells, Auditory, Outer/physiology ; In Vitro Techniques ; Ion Transport ; Male ; Mechanotransduction, Cellular ; Models, Biological ; Molecular Motor Proteins/physiology ; Patch-Clamp Techniques ; Sulfates/metabolism
Chemical Substances	Anions ; Antiporters ; Chlorides ; Molecular Motor Proteins ; Sulfates
Language	English
Publishing date	2006-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218078-9
ISSN	1542-0086 ; 0006-3495
ISSN (online)	1542-0086
ISSN	0006-3495
DOI	10.1529/biophysj.105.073254
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Zs.A 235: 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)
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Article ; Online: Mutant cycles at CFTR's non-canonical ATP-binding site support little interface separation during gating.

Szollosi, Andras / Muallem, Daniella R / Csanády, László / Vergani, Paola

The Journal of general physiology

2011 Volume 137, Issue 6, Page(s) 549–562

Abstract: Cystic fibrosis transmembrane conductance regulator (CFTR) is a chloride channel belonging to the adenosine triphosphate (ATP)-binding cassette (ABC) superfamily. ABC proteins share a common molecular mechanism that couples ATP binding and hydrolysis at ... ...

Abstract	Cystic fibrosis transmembrane conductance regulator (CFTR) is a chloride channel belonging to the adenosine triphosphate (ATP)-binding cassette (ABC) superfamily. ABC proteins share a common molecular mechanism that couples ATP binding and hydrolysis at two nucleotide-binding domains (NBDs) to diverse functions. This involves formation of NBD dimers, with ATP bound at two composite interfacial sites. In CFTR, intramolecular NBD dimerization is coupled to channel opening. Channel closing is triggered by hydrolysis of the ATP molecule bound at composite site 2. Site 1, which is non-canonical, binds nucleotide tightly but is not hydrolytic. Recently, based on kinetic arguments, it was suggested that this site remains closed for several gating cycles. To investigate movements at site 1 by an independent technique, we studied changes in thermodynamic coupling between pairs of residues on opposite sides of this site. The chosen targets are likely to interact based on both phylogenetic analysis and closeness on structural models. First, we mutated T460 in NBD1 and L1353 in NBD2 (the corresponding site-2 residues become energetically coupled as channels open). Mutation T460S accelerated closure in hydrolytic conditions and in the nonhydrolytic K1250R background; mutation L1353M did not affect these rates. Analysis of the double mutant showed additive effects of mutations, suggesting that energetic coupling between the two residues remains unchanged during the gating cycle. We next investigated pairs 460-1348 and 460-1375. Although both mutations H1348A and H1375A produced dramatic changes in hydrolytic and nonhydrolytic channel closing rates, in the corresponding double mutants these changes proved mostly additive with those caused by mutation T460S, suggesting little change in energetic coupling between either positions 460-1348 or positions 460-1375 during gating. These results provide independent support for a gating model in which ATP-bound composite site 1 remains closed throughout the gating cycle.
MeSH term(s)	Action Potentials ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; Cystic Fibrosis Transmembrane Conductance Regulator/chemistry ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Female ; Ion Channel Gating/physiology ; Models, Molecular ; Mutation ; Oocytes/physiology ; Protein Binding ; Protein Conformation ; Xenopus laevis
Chemical Substances	Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2011-05-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3118-5
ISSN	1540-7748 ; 0022-1295
ISSN (online)	1540-7748
ISSN	0022-1295
DOI	10.1085/jgp.201110608
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Article ; Online: Orai1-Mediated Antimicrobial Secretion from Pancreatic Acini Shapes the Gut Microbiome and Regulates Gut Innate Immunity.

Ahuja, Malini / Schwartz, Daniella M / Tandon, Mayank / Son, Aran / Zeng, Mei / Swaim, William / Eckhaus, Michael / Hoffman, Victoria / Cui, Yiyuan / Xiao, Bo / Worley, Paul F / Muallem, Shmuel

Cell metabolism

2017 Volume 25, Issue 3, Page(s) 635–646

Abstract: The gut microbiome participates in numerous physiologic functions and communicates intimately with the host immune system. Antimicrobial peptides are critical components of intestinal innate immunity. We report a prominent role for antimicrobials ... ...

Abstract	The gut microbiome participates in numerous physiologic functions and communicates intimately with the host immune system. Antimicrobial peptides are critical components of intestinal innate immunity. We report a prominent role for antimicrobials secreted by pancreatic acini in shaping the gut microbiome that is essential for intestinal innate immunity, barrier function, and survival. Deletion of the Ca
MeSH term(s)	Acinar Cells/metabolism ; Animals ; Anti-Infective Agents/metabolism ; Calcium Signaling ; Cell Death ; Exocytosis ; Gastrointestinal Microbiome ; Gastrointestinal Tract/immunology ; Gastrointestinal Tract/metabolism ; Gene Deletion ; Homeostasis ; Immunity, Innate ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Intestines/microbiology ; Intestines/pathology ; Mice ; Microbial Viability ; ORAI1 Protein/deficiency ; ORAI1 Protein/metabolism ; Pancreas/cytology ; Protein Biosynthesis
Chemical Substances	Anti-Infective Agents ; Inflammation Mediators ; ORAI1 Protein ; Orai1 protein, mouse
Language	English
Publishing date	2017-03-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2017.02.007
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Article ; Online: Type I interferon signature predicts response to JAK inhibition in haploinsufficiency of A20.

Schwartz, Daniella Muallem / Blackstone, Sarah A / Sampaio-Moura, Natalia / Rosenzweig, Sofia / Burma, Aarohan M / Stone, Deborah / Hoffmann, Patrycja / Jones, Anne / Romeo, Tina / Barron, Karyl S / Waldman, Meryl A / Aksentijevich, Ivona / Kastner, Daniel L / Milner, Joshua D / Ombrello, Amanda K

Annals of the rheumatic diseases

2019 Volume 79, Issue 3, Page(s) 429–431

MeSH term(s)	Adolescent ; Adult ; Female ; Haploinsufficiency/drug effects ; Humans ; Interferon Type I/metabolism ; Janus Kinase Inhibitors/pharmacology ; Loss of Function Mutation/drug effects ; Male ; Middle Aged ; NF-kappa B/metabolism ; Signal Transduction/drug effects ; Tumor Necrosis Factor alpha-Induced Protein 3/genetics ; Young Adult
Chemical Substances	Interferon Type I ; Janus Kinase Inhibitors ; NF-kappa B ; TNFAIP3 protein, human (EC 3.4.19.12) ; Tumor Necrosis Factor alpha-Induced Protein 3 (EC 3.4.19.12)
Language	English
Publishing date	2019-11-25
Publishing country	England
Document type	Letter ; Research Support, N.I.H., Intramural
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/annrheumdis-2019-215918
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