Jonathan Soboloff
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View article: Targeting TRPC channels for control of arthritis-induced bone erosion
Targeting TRPC channels for control of arthritis-induced bone erosion Open
Arthritis leads to bone erosion due to an imbalance between osteoclast and osteoblast function. Our prior investigations revealed that the Ca 2+ -selective ion channel, Orai1, is critical for osteoclast maturation. Here, we show that the s…
View article: TPC2 controls MITF expression and metastasis in melanoma
TPC2 controls MITF expression and metastasis in melanoma Open
Recent findings by Abrahamian et al. (2024) provides new insights into the relationship between Two Pore Channel 2 (TPC2) activity and the development and progression of melanoma. Melanocyte inducing transcription factor (MITF) is a critic…
View article: Enforced Expression of Mitochondrial Calcium Uniporter in Donor T Cells Abolishes Gvhd Progression
Enforced Expression of Mitochondrial Calcium Uniporter in Donor T Cells Abolishes Gvhd Progression Open
During the early/intermediate phases of the immune response, calcium (Ca2+) signals are crucial for T cell activation, proliferation and effector differentiation. Yet, inhibiting Ca2+ signaling-activated master transcription factor NFAT ha…
View article: Molecular Regulation of Bone Turnover in Juvenile Idiopathic Arthritis: Animal Models, Cellular Features and TNFα
Molecular Regulation of Bone Turnover in Juvenile Idiopathic Arthritis: Animal Models, Cellular Features and TNFα Open
We review the abnormal bone turnover that is the basis of idiopathic inflammatory or rheumatoid arthritis and bone loss, with emphasis on Tumor Necrosis Factor-alpha (TNFα)-related mechanisms. We review selected data on idiopathic arthriti…
View article: Preclinical evaluation of ELP‐004 in mice
Preclinical evaluation of ELP‐004 in mice Open
This study provides a detailed understanding of the preclinical pharmacokinetics and metabolism of ELP‐004, an osteoclast inhibitor in development for the treatment of bone erosion. Current treatments for arthritis, including biological di…
View article: Dual Functions of Mitochondrial Calcium Uniporter in T Cell Alloimmunity
Dual Functions of Mitochondrial Calcium Uniporter in T Cell Alloimmunity Open
Despite pharmacological prophylaxis using calcineurin inhibitors, graft-versus-host disease (GVHD) still occurs in patients undergoing allogeneic hematopoietic stem cell transplantation. However, the mechanism that underlies the breakthrou…
View article: Trogocytosis of cancer-associated fibroblasts promotes pancreatic cancer growth and immune suppression via phospholipid scramblase anoctamin 6 (ANO6)
Trogocytosis of cancer-associated fibroblasts promotes pancreatic cancer growth and immune suppression via phospholipid scramblase anoctamin 6 (ANO6) Open
In pancreatic ductal adenocarcinoma (PDAC), the fibroblastic stroma constitutes most of the tumor mass and is remarkably devoid of functional blood vessels. This raises an unresolved question of how PDAC cells obtain essential metabolites …
View article: EGR4 is critical for cell-fate determination and phenotypic maintenance of geniculate ganglion neurons underlying sweet and umami taste
EGR4 is critical for cell-fate determination and phenotypic maintenance of geniculate ganglion neurons underlying sweet and umami taste Open
The sense of taste starts with activation of receptor cells in taste buds by chemical stimuli which then communicate this signal via innervating oral sensory neurons to the CNS. The cell bodies of oral sensory neurons reside in the genicul…
View article: The calcium channel Orai1 is required for osteoblast development: Studies in a chimeric mouse with variable in vivo Runx-cre deletion of Orai-1
The calcium channel Orai1 is required for osteoblast development: Studies in a chimeric mouse with variable in vivo Runx-cre deletion of Orai-1 Open
The calcium-selective ion channel Orai1 has a complex role in bone homeostasis, with defects in both bone production and resorption detected in Orai1 germline knock-out mice. To determine whether Orai1 has a direct, cell-intrinsic role in …
View article: Supplementary Figures S1-S7 from Interferon-γ Signaling in Melanocytes and Melanoma Cells Regulates Expression of CTLA-4
Supplementary Figures S1-S7 from Interferon-γ Signaling in Melanocytes and Melanoma Cells Regulates Expression of CTLA-4 Open
Supplementary Figure S1: CTLA4 mRNA expression in human tumor cell lines. Supplementary Figure S2: CTLA4 promoter analysis. Supplementary Figure S3: UCSC genome browser view of human CTLA4 locus. Supplementary Figure S4: Recruitment of STA…
View article: Supplementary Figures S1-S7 from Interferon-γ Signaling in Melanocytes and Melanoma Cells Regulates Expression of CTLA-4
Supplementary Figures S1-S7 from Interferon-γ Signaling in Melanocytes and Melanoma Cells Regulates Expression of CTLA-4 Open
Supplementary Figure S1: CTLA4 mRNA expression in human tumor cell lines. Supplementary Figure S2: CTLA4 promoter analysis. Supplementary Figure S3: UCSC genome browser view of human CTLA4 locus. Supplementary Figure S4: Recruitment of STA…
View article: Data from Interferon-γ Signaling in Melanocytes and Melanoma Cells Regulates Expression of CTLA-4
Data from Interferon-γ Signaling in Melanocytes and Melanoma Cells Regulates Expression of CTLA-4 Open
CTLA4 is a cell surface receptor on T cells that functions as an immune checkpoint molecule to enforce tolerance to cognate antigens. Anti–CTLA4 immunotherapy is highly effective at reactivating T-cell responses against melanoma, which is …
View article: Data from Interferon-γ Signaling in Melanocytes and Melanoma Cells Regulates Expression of CTLA-4
Data from Interferon-γ Signaling in Melanocytes and Melanoma Cells Regulates Expression of CTLA-4 Open
CTLA4 is a cell surface receptor on T cells that functions as an immune checkpoint molecule to enforce tolerance to cognate antigens. Anti–CTLA4 immunotherapy is highly effective at reactivating T-cell responses against melanoma, which is …
View article: Disruption of <scp>Mitochondrial‐associated ER</scp> membranes by <scp>HIV</scp>‐1 tat protein contributes to premature brain aging
Disruption of <span>Mitochondrial‐associated ER</span> membranes by <span>HIV</span>‐1 tat protein contributes to premature brain aging Open
Introduction Mitochondrial‐associated ER membranes (MAMs) control many cellular functions, including calcium and lipid exchange, intracellular trafficking, and mitochondrial biogenesis. The disruption of these functions contributes to neur…
View article: The ERK2 DBP domain opposes pathogenesis of a JAK2V617F-driven myeloproliferative neoplasm
The ERK2 DBP domain opposes pathogenesis of a JAK2V617F-driven myeloproliferative neoplasm Open
While Ras/mitogen-activated protein kinase (MAPK) signaling is activated in most human cancers, attempts to target this pathway using kinase active site inhibitors have not typically led to durable, clinical benefit. To address this shortc…
View article: The calcium channel Orai1 is required for osteoblast development: studies in a chimeric mouse with variable <i>in vivo</i> Runx-cre deletion of Orai-1
The calcium channel Orai1 is required for osteoblast development: studies in a chimeric mouse with variable <i>in vivo</i> Runx-cre deletion of Orai-1 Open
The calcium-selective ion channel Orai1 has a complex role in bone homeostasis, with defects in both bone production and resorption detected in Orai1 germline knock-out mice. To determine whether Orai1 has a direct, cell-intrinsic role in …
View article: The function of the calcium channel Orai1 in osteoclast development
The function of the calcium channel Orai1 in osteoclast development Open
To determine the intrinsic role of Orai1 in osteoclast development, Orai1‐floxed mice were bred with LysMcre mice to delete Orai1 from the myeloid lineage. PCR, in situ labelling and Western analysis showed Orai1 deletion in myeloid‐lineag…
View article: Mitochondrial pyruvate and fatty acid flux modulate MICU1-dependent control of MCU activity
Mitochondrial pyruvate and fatty acid flux modulate MICU1-dependent control of MCU activity Open
Nutrient stress triggers transcriptional changes that limit Ca 2+ influx into mitochondria through the MCU.