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Article ; Online: Structural and Biophysical Analysis of the CLCA1 VWA Domain Suggests Mode of TMEM16A Engagement.

Berry, Kayla N / Brett, Tom J

2020 Volume 30, Issue 4, Page(s) 1141–1151.e3

Abstract: The secreted protein calcium-activated chloride channel regulator 1 (CLCA1) utilizes a von Willebrand factor type A (VWA) domain to bind to and potentiate the calcium-activated chloride channel TMEM16A. To gain insight into this unique potentiation ... ...

Abstract	The secreted protein calcium-activated chloride channel regulator 1 (CLCA1) utilizes a von Willebrand factor type A (VWA) domain to bind to and potentiate the calcium-activated chloride channel TMEM16A. To gain insight into this unique potentiation mechanism, we determined the 2.0-Å crystal structure of human CLCA1 VWA bound to Ca
MeSH term(s)	Anoctamin-1/chemistry ; Anoctamin-1/metabolism ; Biophysical Phenomena ; Chloride Channels/chemistry ; Chloride Channels/metabolism ; Crystallography, X-Ray ; Humans ; Models, Molecular ; Neoplasm Proteins/chemistry ; Neoplasm Proteins/metabolism ; Protein Domains ; Protein Folding
Chemical Substances	ANO1 protein, human ; Anoctamin-1 ; CLCA1 protein, human ; Chloride Channels ; Neoplasm Proteins
Language	English
Publishing date	2020-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.12.059
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Article ; Online: Limiting Respiratory Viral Infection by Targeting Antiviral and Immunological Functions of BST-2/Tetherin: Knowledge and Gaps.

Berry, Kayla N / Kober, Daniel L / Su, Alvin / Brett, Tom J

BioEssays : news and reviews in molecular, cellular and developmental biology

2018 Volume 40, Issue 10, Page(s) e1800086

Abstract: Recent findings regarding the cellular biology and immunology of BST-2 (also known as tetherin) indicate that its function could be exploited as a universal replication inhibitor of enveloped respiratory viruses (e.g., influenza, respiratory syncytial ... ...

Abstract	Recent findings regarding the cellular biology and immunology of BST-2 (also known as tetherin) indicate that its function could be exploited as a universal replication inhibitor of enveloped respiratory viruses (e.g., influenza, respiratory syncytial virus, etc.). BST-2 inhibits viral replication by preventing virus budding from the plasma membrane and by inducing an antiviral state in cells adjacent to infection via unique inflammatory signaling mechanisms. This review presents the first comprehensive summary of what is currently known about BST-2 anti-viral function against respiratory viruses, how these viruses construct countermeasures to antagonize BST-2, and how BST-2 function might be targeted to develop therapies to treat respiratory virus infections. The authors address the current gaps in knowledge, including the need for mechanistic understanding of BST-2 antagonism by respiratory viruses, that should be bridged to achieve that goal.
MeSH term(s)	Antigens, CD/chemistry ; Antigens, CD/physiology ; GPI-Linked Proteins/antagonists & inhibitors ; GPI-Linked Proteins/chemistry ; GPI-Linked Proteins/physiology ; Host-Pathogen Interactions/physiology ; Humans ; Molecular Targeted Therapy/methods ; Respiratory Tract Infections/virology ; Signal Transduction ; Virion ; Virus Diseases/immunology ; Virus Release ; Virus Replication/drug effects
Chemical Substances	Antigens, CD ; BST2 protein, human ; GPI-Linked Proteins
Keywords	covid19
Language	English
Publishing date	2018-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.201800086
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Article: Limiting Respiratory Viral Infection by Targeting Antiviral and Immunological Functions of BST‐2/Tetherin: Knowledge and Gaps

Berry, Kayla N / Kober, Daniel L / Su, Alvin / Brett, Tom J

BioEssays. 2018 Oct., v. 40, no. 10

2018

Abstract: Recent findings regarding the cellular biology and immunology of BST‐2 (also known as tetherin) indicate that its function could be exploited as a universal replication inhibitor of enveloped respiratory viruses (e.g., influenza, respiratory syncytial ... ...

Abstract	Recent findings regarding the cellular biology and immunology of BST‐2 (also known as tetherin) indicate that its function could be exploited as a universal replication inhibitor of enveloped respiratory viruses (e.g., influenza, respiratory syncytial virus, etc.). BST‐2 inhibits viral replication by preventing virus budding from the plasma membrane and by inducing an antiviral state in cells adjacent to infection via unique inflammatory signaling mechanisms. This review presents the first comprehensive summary of what is currently known about BST‐2 anti‐viral function against respiratory viruses, how these viruses construct countermeasures to antagonize BST‐2, and how BST‐2 function might be targeted to develop therapies to treat respiratory virus infections. The authors address the current gaps in knowledge, including the need for mechanistic understanding of BST‐2 antagonism by respiratory viruses, that should be bridged to achieve that goal.
Keywords	Respiratory syncytial virus ; antagonism ; immunology ; influenza ; plasma membrane ; virus replication ; viruses ; covid19
Language	English
Dates of publication	2018-10
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.201800086
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Article ; Online: Alpha herpesvirus exocytosis from neuron cell bodies uses constitutive secretory mechanisms, and egress and spread from axons is independent of neuronal firing activity.

Ambrosini, Anthony E / Borg, Kayla M / Deshmukh, Nikhil / Berry, Michael J / Enquist, Lynn W / Hogue, Ian B

PLoS pathogens

2024 Volume 20, Issue 4, Page(s) e1012139

Abstract: Alpha herpesviruses naturally infect the peripheral nervous system, and can spread to the central nervous system, causing severe debilitating or deadly disease. Because alpha herpesviruses spread along synaptic circuits, and infected neurons exhibit ... ...

Abstract	Alpha herpesviruses naturally infect the peripheral nervous system, and can spread to the central nervous system, causing severe debilitating or deadly disease. Because alpha herpesviruses spread along synaptic circuits, and infected neurons exhibit altered electrophysiology and increased spontaneous activity, we hypothesized that alpha herpesviruses use activity-dependent synaptic vesicle-like regulated secretory mechanisms for egress and spread from neurons. Using live-cell fluorescence microscopy, we show that Pseudorabies Virus (PRV) particles use the constitutive Rab6 post-Golgi secretory pathway to exit from the cell body of primary neurons, independent of local calcium signaling. Some PRV particles colocalize with Rab6 in the proximal axon, but we did not detect colocalization/co-transport in the distal axon. Thus, the specific secretory mechanisms used for viral egress from axons remains unclear. To address the role of neuronal activity more generally, we used a compartmentalized neuron culture system to measure the egress and spread of PRV from axons, and pharmacological and optogenetics approaches to modulate neuronal activity. Using tetrodotoxin to silence neuronal activity, we observed no inhibition, and using potassium chloride or optogenetics to elevate neuronal activity, we also show no increase in virus spread from axons. We conclude that PRV egress from neurons uses constitutive secretory mechanisms: generally, activity-independent mechanisms in axons, and specifically, the constitutive Rab6 post-Golgi secretory pathway in cell bodies.
MeSH term(s)	Animals ; Cell Body/metabolism ; Viral Envelope Proteins/metabolism ; Axons ; Alphaherpesvirinae/metabolism ; Neurons ; Herpesvirus 1, Suid/metabolism ; Pseudorabies/metabolism ; Exocytosis
Chemical Substances	Viral Envelope Proteins
Language	English
Publishing date	2024-04-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1012139
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Article ; Online: Melanomas with concurrent BRAF non-p.V600 and NF1 loss-of-function mutations are targetable by BRAF/MEK inhibitor combination therapy.

Rajkumar, Shivshankari / Berry, Diana / Heney, Kayla A / Strong, Colton / Ramsay, LeeAnn / Lajoie, Mathieu / Alkallas, Rached / Nguyen, Tan-Trieu / Thomson, Cameron / Ahanfeshar-Adams, Mozhdeh / Dankner, Matthew / Petrella, Teresa / Rose, April A N / Siegel, Peter M / Watson, Ian R

Cell reports

2022 Volume 39, Issue 1, Page(s) 110634

Abstract: Although combination BRAF/MEK inhibition has produced significant survival benefits for BRAF p.V600 mutant melanomas, targeted therapies approved for BRAF non-p.V600 mutant melanomas remain limited. Through the analysis of 772 cutaneous melanoma exomes, ... ...

Abstract	Although combination BRAF/MEK inhibition has produced significant survival benefits for BRAF p.V600 mutant melanomas, targeted therapies approved for BRAF non-p.V600 mutant melanomas remain limited. Through the analysis of 772 cutaneous melanoma exomes, we reveal that BRAF non-p.V600 mutations co-occurs more frequently with NF1 loss, but not with oncogenic NRAS mutations, than expected by chance. We present cell signaling data, which demonstrate that BRAF non-p.V600 mutants can signal as monomers and dimers within an NF1 loss context. Concordantly, BRAF inhibitors that inhibit both monomeric and dimeric BRAF synergize with MEK inhibition to significantly reduce cell viability in vitro and tumor growth in vivo in BRAF non-p.V600 mutant melanomas with co-occurring NF1 loss-of-function mutations. Our data suggest that patients harboring BRAF non-p.V600 mutant melanomas may benefit from current FDA-approved BRAF/MEK inhibitor combination therapy currently reserved for BRAF p.V600 mutant patients.
MeSH term(s)	Humans ; Melanoma/drug therapy ; Melanoma/genetics ; Mitogen-Activated Protein Kinase Kinases/genetics ; Mutation/genetics ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Proto-Oncogene Proteins B-raf/genetics ; Skin Neoplasms/drug therapy ; Skin Neoplasms/genetics
Chemical Substances	Protein Kinase Inhibitors ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
Language	English
Publishing date	2022-04-06
Publishing country	United States
Document type	Journal Article ; 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.2022.110634
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Article ; Online: Melanomas with concurrent BRAF non-p.V600 and NF1 loss-of-function mutations are targetable by BRAF/MEK inhibitor combination therapy

Shivshankari Rajkumar / Diana Berry / Kayla A. Heney / Colton Strong / LeeAnn Ramsay / Mathieu Lajoie / Rached Alkallas / Tan-Trieu Nguyen / Cameron Thomson / Mozhdeh Ahanfeshar-Adams / Matthew Dankner / Teresa Petrella / April A.N. Rose / Peter M. Siegel / Ian R. Watson

Cell Reports, Vol 39, Iss 1, Pp 110634- (2022)

2022

Abstract: Summary: Although combination BRAF/MEK inhibition has produced significant survival benefits for BRAF p.V600 mutant melanomas, targeted therapies approved for BRAF non-p.V600 mutant melanomas remain limited. Through the analysis of 772 cutaneous melanoma ...

Abstract	Summary: Although combination BRAF/MEK inhibition has produced significant survival benefits for BRAF p.V600 mutant melanomas, targeted therapies approved for BRAF non-p.V600 mutant melanomas remain limited. Through the analysis of 772 cutaneous melanoma exomes, we reveal that BRAF non-p.V600 mutations co-occurs more frequently with NF1 loss, but not with oncogenic NRAS mutations, than expected by chance. We present cell signaling data, which demonstrate that BRAF non-p.V600 mutants can signal as monomers and dimers within an NF1 loss context. Concordantly, BRAF inhibitors that inhibit both monomeric and dimeric BRAF synergize with MEK inhibition to significantly reduce cell viability in vitro and tumor growth in vivo in BRAF non-p.V600 mutant melanomas with co-occurring NF1 loss-of-function mutations. Our data suggest that patients harboring BRAF non-p.V600 mutant melanomas may benefit from current FDA-approved BRAF/MEK inhibitor combination therapy currently reserved for BRAF p.V600 mutant patients.
Keywords	CP: Cancer ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Novel Roles for Chloride Channels, Exchangers, and Regulators in Chronic Inflammatory Airway Diseases.

Sala-Rabanal, Monica / Yurtsever, Zeynep / Berry, Kayla N / Brett, Tom J

Mediators of inflammation

2015 Volume 2015, Page(s) 497387

Abstract: Chloride transport proteins play critical roles in inflammatory airway diseases, contributing to the detrimental aspects of mucus overproduction, mucus secretion, and airway constriction. However, they also play crucial roles in contributing to the ... ...

Abstract	Chloride transport proteins play critical roles in inflammatory airway diseases, contributing to the detrimental aspects of mucus overproduction, mucus secretion, and airway constriction. However, they also play crucial roles in contributing to the innate immune properties of mucus and mucociliary clearance. In this review, we focus on the emerging novel roles for a chloride channel regulator (CLCA1), a calcium-activated chloride channel (TMEM16A), and two chloride exchangers (SLC26A4/pendrin and SLC26A9) in chronic inflammatory airway diseases.
MeSH term(s)	Anoctamin-1 ; Antiporters/physiology ; Asthma/etiology ; Chloride Channels/physiology ; Cystic Fibrosis Transmembrane Conductance Regulator/physiology ; Humans ; Membrane Transport Proteins/physiology ; Neoplasm Proteins/physiology ; Pulmonary Disease, Chronic Obstructive/etiology ; STAT6 Transcription Factor/physiology
Chemical Substances	ANO1 protein, human ; Anoctamin-1 ; Antiporters ; CLCA1 protein, human ; Chloride Channels ; Membrane Transport Proteins ; Neoplasm Proteins ; SLC26A4 protein, human ; SLC26A9 protein, human ; STAT6 Transcription Factor ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2015/497387
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Article ; Online: Modulation of TMEM16A channel activity by the von Willebrand factor type A (VWA) domain of the calcium-activated chloride channel regulator 1 (CLCA1).

Sala-Rabanal, Monica / Yurtsever, Zeynep / Berry, Kayla N / Nichols, Colin G / Brett, Tom J

The Journal of biological chemistry

2017 Volume 292, Issue 22, Page(s) 9164–9174

Abstract: ... Willebrand factor type A (VWA) domain within the cleaved CLCA1 N-terminal fragment is necessary and ...

Abstract	Calcium-activated chloride channels (CaCCs) are key players in transepithelial ion transport and fluid secretion, smooth muscle constriction, neuronal excitability, and cell proliferation. The CaCC regulator 1 (CLCA1) modulates the activity of the CaCC TMEM16A/Anoctamin 1 (ANO1) by directly engaging the channel at the cell surface, but the exact mechanism is unknown. Here we demonstrate that the von Willebrand factor type A (VWA) domain within the cleaved CLCA1 N-terminal fragment is necessary and sufficient for this interaction. TMEM16A protein levels on the cell surface were increased in HEK293T cells transfected with CLCA1 constructs containing the VWA domain, and TMEM16A-like currents were activated. Similar currents were evoked in cells exposed to secreted VWA domain alone, and these currents were significantly knocked down by TMEM16A siRNA. VWA-dependent TMEM16A modulation was not modified by the S357N mutation, a VWA domain polymorphism associated with more severe meconium ileus in cystic fibrosis patients. VWA-activated currents were significantly reduced in the absence of extracellular Mg
MeSH term(s)	Amino Acid Substitution ; Anoctamin-1 ; Cell Line ; Chloride Channels/genetics ; Chloride Channels/metabolism ; Humans ; Magnesium/metabolism ; Mutation, Missense ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Protein Domains ; Protein Stability
Chemical Substances	ANO1 protein, human ; Anoctamin-1 ; CLCA1 protein, human ; Chloride Channels ; Neoplasm Proteins ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2017-04-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M117.788232
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Article ; Online: Psychologic assessment in patients undergoing bariatric surgery.

Ferrin, Neal / Elian, Alain / Flewelling, Kayla / Nadeem, Muhammed / Nava, Kristofer / Berry, Shamsi Daneshvari / Stehlik, Kevin / Bella, Almontasser Kassier / Awad, Peter / Alfred, Andrew / Ksajikian, Andre / Chen, Kevin / Shebrain, Saad

Surgical endoscopy

2024 Volume 38, Issue 4, Page(s) 1922–1932

Abstract: Background: Psychological Clearance level (PCL) for patients undergoing metabolic and bariatric surgery (MBS) is a critical step for successful postoperative outcomes. This study aims to assess the relationship between the level of psychologic fitness ... ...

Abstract	Background: Psychological Clearance level (PCL) for patients undergoing metabolic and bariatric surgery (MBS) is a critical step for successful postoperative outcomes. This study aims to assess the relationship between the level of psychologic fitness and postoperative outcomes in patients undergoing MBS. Methods: We retrospectively analyzed the data of patients who underwent MBS (laparoscopic sleeve gastrectomy [LSG] and laparoscopic Roux-en-Y Gastric Bypass [LRYGB]) and completed two years follow-up, between 2012 and 2019, in a single medical center. The patients were divided into four groups based on PCL, suggesting level of readiness for surgery: Group A (PCL-0: guarded), group B (PCL-1: Fair/reasonable), group C (PCL-2: Good/appropriate), and group D (PCL-3: Strong/excellent). Primary outcome was the percent of total body weight loss (%TWL), and the absolute change in BMI units. Secondary outcomes were missed postoperative visits and patient compliance. Differences between the groups were analyzed using a generalized linear model (GLM), chi-squared and exact Fisher tests, as appropriate. Results: Of 1411 total patients, 607 (43.20%) had complete data at two years follow-up. 512 (84.34%) were females. LSG was performed in 361 (59.5%). No difference was found in %TWL between the four groups (22.14% vs. 28.0% vs. 26.0% vs. 24.8%, p = 0.118). We found a small difference in the mean (SD) of absolute change in BMI between the groups, and on post-hoc analysis it was found between groups B (PCL-1) and D (PCL-3). Overall, no difference between the groups in number of follow-up visits, or compliance issues. However, patients who attended more follow-up visits had less compliance issues (p < 0.001). PCL is inversely correlated with number of psychologic diagnoses (r = - 0.41, p < 0.001) and medical comorbidities (r = - 0.20, p < 0.001). Conclusion: We found no difference in the percent of TWL in patients who underwent MBS based on PCL at two -years follow-up. Medical comorbidities and psychiatric diagnoses impact the PCL.
MeSH term(s)	Female ; Humans ; Male ; Obesity, Morbid/surgery ; Retrospective Studies ; Weight Loss ; Treatment Outcome ; Gastric Bypass/adverse effects ; Bariatric Surgery ; Laparoscopy/adverse effects ; Gastrectomy/adverse effects
Language	English
Publishing date	2024-02-08
Publishing country	Germany
Document type	Journal Article
ZDB-ID	639039-0
ISSN	1432-2218 ; 0930-2794
ISSN (online)	1432-2218
ISSN	0930-2794
DOI	10.1007/s00464-023-10668-9
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Article ; Online: A Polycomb complex remains bound through DNA replication in the absence of other eukaryotic proteins.

Lengsfeld, Bettina M / Berry, Kayla N / Ghosh, Sharmistha / Takahashi, Masateru / Francis, Nicole J

Scientific reports

2012 Volume 2, Page(s) 661

Abstract: Propagation of chromatin states through DNA replication is central to epigenetic regulation and can involve recruitment of chromatin proteins to replicating chromatin through interactions with replication fork components. Here we show using a fully ... ...

Abstract	Propagation of chromatin states through DNA replication is central to epigenetic regulation and can involve recruitment of chromatin proteins to replicating chromatin through interactions with replication fork components. Here we show using a fully reconstituted T7 bacteriophage system that eukaryotic proteins are not required to tether the Polycomb complex PRC1 to templates during DNA replication. Instead, DNA binding by PRC1 can withstand passage of a simple replication fork.
MeSH term(s)	Bacteriophage T7/genetics ; Binding, Competitive ; DNA Helicases/chemistry ; DNA Replication ; DNA, Viral/chemistry ; DNA-Directed DNA Polymerase/chemistry ; Plasmids/chemistry ; Polycomb-Group Proteins/chemistry ; Protein Binding ; Viral Proteins/chemistry
Chemical Substances	DNA, Viral ; Polycomb-Group Proteins ; Viral Proteins ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; DNA Helicases (EC 3.6.4.-)
Language	English
Publishing date	2012-09-17
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/srep00661
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