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Showing 1 to 12 of 45 entries
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VEGF signaling, mTOR complexes, and the endoplasmic reticulum: Towards a role of metabolic sensing in the regulation of angiogenesis.

Molecular & cellular oncology

Karali E, Bellou S, Stellas D, Klinakis A, Murphy C, Fotsis T.
PMID: 27308350
Mol Cell Oncol. 2014 Dec 23;1(3):e964024. doi: 10.4161/23723548.2014.964024. eCollection 2014.

Vascular endothelial growth factor (VEGF) activates unfolded protein response sensors in the endoplasmic reticulum through phospholipase C gamma (PLCγ)-mediated crosstalk with mammalian target of rapamycin complex 1 (mTORC1). Activation of transcription factor 6 (ATF6) and protein kinase RNA-like endoplasmic...

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Karali E, Bellou S, Stellas D, et al. VEGF signaling, mTOR complexes, and the endoplasmic reticulum: Towards a role of metabolic sensing in the regulation of angiogenesis. Mol Cell Oncol. 2014;1(3):e964024doi: 10.4161/23723548.2014.964024.
Karali, E., Bellou, S., Stellas, D., Klinakis, A., Murphy, C., & Fotsis, T. (2014). VEGF signaling, mTOR complexes, and the endoplasmic reticulum: Towards a role of metabolic sensing in the regulation of angiogenesis. Molecular & cellular oncology, 1(3), e964024. https://doi.org/10.4161/23723548.2014.964024
Karali, Evdoxia, et al. "VEGF signaling, mTOR complexes, and the endoplasmic reticulum: Towards a role of metabolic sensing in the regulation of angiogenesis." Molecular & cellular oncology vol. 1,3 (2014): e964024. doi: https://doi.org/10.4161/23723548.2014.964024
Karali E, Bellou S, Stellas D, Klinakis A, Murphy C, Fotsis T. VEGF signaling, mTOR complexes, and the endoplasmic reticulum: Towards a role of metabolic sensing in the regulation of angiogenesis. Mol Cell Oncol. 2014 Dec 23;1(3):e964024. doi: 10.4161/23723548.2014.964024. eCollection 2014. PMID: 27308350; PMCID: PMC4904886.
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Interferon-gamma increases neuronal death in response to amyloid-beta1-42.

Journal of neuroinflammation

Bate C, Kempster S, Last V, Williams A.
PMID: 16569229
J Neuroinflammation. 2006 Mar 28;3:7. doi: 10.1186/1742-2094-3-7.

BACKGROUND: Alzheimer's disease is a neurodegenerative disorder characterized by a progressive cognitive impairment, the consequence of neuronal dysfunction and ultimately the death of neurons. The amyloid hypothesis proposes that neuronal damage results from the accumulation of insoluble, hydrophobic, fibrillar...

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Bate C, Kempster S, Last V, et al. Interferon-gamma increases neuronal death in response to amyloid-beta1-42. J Neuroinflammation. 2006;3:7doi: 10.1186/1742-2094-3-7.
Bate, C., Kempster, S., Last, V., & Williams, A. (2006). Interferon-gamma increases neuronal death in response to amyloid-beta1-42. Journal of neuroinflammation, 37. https://doi.org/10.1186/1742-2094-3-7
Bate, Clive, et al. "Interferon-gamma increases neuronal death in response to amyloid-beta1-42." Journal of neuroinflammation vol. 3 (2006): 7. doi: https://doi.org/10.1186/1742-2094-3-7
Bate C, Kempster S, Last V, Williams A. Interferon-gamma increases neuronal death in response to amyloid-beta1-42. J Neuroinflammation. 2006 Mar 28;3:7. doi: 10.1186/1742-2094-3-7. PMID: 16569229; PMCID: PMC1435873.
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Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway.

Journal of endocrinology and diabetes

Zimering MB.
PMID: 29805993
J Endocrinol Diabetes. 2017;4(4). doi: 10.15226/2374-6890/4/4/00184. Epub 2017 Oct 04.

AIMS: To identify the G-protein coupled receptor(s) on neuroblastoma and endothelial cells which mediate neural- and endothelial cell-inhibitory effects in plasma autoantibodies from a subset of older type 2 diabetes with neurologic and vascular co-morbidity. To determine the mechanism(s)...

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Zimering MB. Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway. J Endocrinol Diabetes. 2017;4(4)doi: 10.15226/2374-6890/4/4/00184.
Zimering, M. B. (2017). Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway. Journal of endocrinology and diabetes, 4(4), . https://doi.org/10.15226/2374-6890/4/4/00184
Zimering, Mark B. "Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway." Journal of endocrinology and diabetes vol. 4,4 (2017). doi: https://doi.org/10.15226/2374-6890/4/4/00184
Zimering MB. Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway. J Endocrinol Diabetes. 2017;4(4). doi: 10.15226/2374-6890/4/4/00184. Epub 2017 Oct 04. PMID: 29805993; PMCID: PMC5964990.
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The Conformational State of the BTK Substrate PLCγ Contributes to Ibrutinib Resistance.

Journal of molecular biology

Joseph RE, Lowe J, Fulton DB, Engen JR, Wales TE, Andreotti AH.
PMID: 34954235
J Mol Biol. 2021 Dec 23;434(5):167422. doi: 10.1016/j.jmb.2021.167422. Epub 2021 Dec 23.

Mutations in PLCγ, a substrate of the tyrosine kinase BTK, are often found in patients who develop resistance to the BTK inhibitor Ibrutinib. However, the mechanisms by which these PLCγ mutations cause Ibrutinib resistance are unclear. Under normal signaling...

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Joseph RE, Lowe J, Fulton DB, et al. The Conformational State of the BTK Substrate PLCγ Contributes to Ibrutinib Resistance. J Mol Biol. 2021;434(5):167422doi: 10.1016/j.jmb.2021.167422.
Joseph, R. E., Lowe, J., Fulton, D. B., Engen, J. R., Wales, T. E., & Andreotti, A. H. (2021). The Conformational State of the BTK Substrate PLCγ Contributes to Ibrutinib Resistance. Journal of molecular biology, 434(5), 167422. https://doi.org/10.1016/j.jmb.2021.167422
Joseph, Raji E, et al. "The Conformational State of the BTK Substrate PLCγ Contributes to Ibrutinib Resistance." Journal of molecular biology vol. 434,5 (2021): 167422. doi: https://doi.org/10.1016/j.jmb.2021.167422
Joseph RE, Lowe J, Fulton DB, Engen JR, Wales TE, Andreotti AH. The Conformational State of the BTK Substrate PLCγ Contributes to Ibrutinib Resistance. J Mol Biol. 2021 Dec 23;434(5):167422. doi: 10.1016/j.jmb.2021.167422. Epub 2021 Dec 23. PMID: 34954235.
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A novel likely pathogenic PLCG2 variant in a patient with a recurrent skin blistering disease and B-cell lymphopenia.

European journal of medical genetics

Park HS, Oh A, Keum CW, Lee J, Lee JK, Son BR, Shin KS, Hahn YS.
PMID: 34768012
Eur J Med Genet. 2021 Nov 09;65(1):104387. doi: 10.1016/j.ejmg.2021.104387. Epub 2021 Nov 09.

Pathogenic variants of PLCG2 encoding phospholipase C gamma 2 (PLCγ2) were first reported in 2012 and their clinical manifestations vary widely. PLCG2-associated antibody deficiency and immune dysregulation (PLAID) and autoinflammation and PLCγ2-associated antibody deficiency and immune dysregulation (APLAID) are...

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Park HS, Oh A, Keum CW, et al. A novel likely pathogenic PLCG2 variant in a patient with a recurrent skin blistering disease and B-cell lymphopenia. Eur J Med Genet. 2021;65(1):104387doi: 10.1016/j.ejmg.2021.104387.
Park, H. S., Oh, A., Keum, C. W., Lee, J., Lee, J. K., Son, B. R., Shin, K. S., & Hahn, Y. S. (2021). A novel likely pathogenic PLCG2 variant in a patient with a recurrent skin blistering disease and B-cell lymphopenia. European journal of medical genetics, 65(1), 104387. https://doi.org/10.1016/j.ejmg.2021.104387
Park, Hee Sue, et al. "A novel likely pathogenic PLCG2 variant in a patient with a recurrent skin blistering disease and B-cell lymphopenia." European journal of medical genetics vol. 65,1 (2021): 104387. doi: https://doi.org/10.1016/j.ejmg.2021.104387
Park HS, Oh A, Keum CW, Lee J, Lee JK, Son BR, Shin KS, Hahn YS. A novel likely pathogenic PLCG2 variant in a patient with a recurrent skin blistering disease and B-cell lymphopenia. Eur J Med Genet. 2021 Nov 09;65(1):104387. doi: 10.1016/j.ejmg.2021.104387. Epub 2021 Nov 09. PMID: 34768012.
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Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway.

Journal of endocrinology and diabetes

Zimering MB.
PMID: 29805993
J Endocrinol Diabetes. 2017;4(4). doi: 10.15226/2374-6890/4/4/00184. Epub 2017 Oct 04.

AIMS: To identify the G-protein coupled receptor(s) on neuroblastoma and endothelial cells which mediate neural- and endothelial cell-inhibitory effects in plasma autoantibodies from a subset of older type 2 diabetes with neurologic and vascular co-morbidity. To determine the mechanism(s)...

Cite
Zimering MB. Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway. J Endocrinol Diabetes. 2017;4(4)doi: 10.15226/2374-6890/4/4/00184.
Zimering, M. B. (2017). Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway. Journal of endocrinology and diabetes, 4(4), . https://doi.org/10.15226/2374-6890/4/4/00184
Zimering, Mark B. "Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway." Journal of endocrinology and diabetes vol. 4,4 (2017). doi: https://doi.org/10.15226/2374-6890/4/4/00184
Zimering MB. Diabetes Autoantibodies Mediate Neural- and Endothelial Cell- Inhibitory Effects Via 5-Hydroxytryptamine- 2 Receptor Coupled to Phospholipase C/Inositol Triphosphate/Ca2+ Pathway. J Endocrinol Diabetes. 2017;4(4). doi: 10.15226/2374-6890/4/4/00184. Epub 2017 Oct 04. PMID: 29805993; PMCID: PMC5964990.
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The role of fibroblast growth factor 8 in cartilage development and disease.

Journal of cellular and molecular medicine

Chen H, Cui Y, Zhang D, Xie J, Zhou X.
PMID: 35001536
J Cell Mol Med. 2022 Jan 09; doi: 10.1111/jcmm.17174. Epub 2022 Jan 09.

Fibroblast growth factor 8 (FGF-8), also known as androgen-induced growth factor (AIGF), is presumed to be a potent mitogenic cytokine that plays important roles in early embryonic development, brain formation and limb development. In the bone environment, FGF-8 produced...

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Chen H, Cui Y, Zhang D, et al. The role of fibroblast growth factor 8 in cartilage development and disease. J Cell Mol Med. 2022;doi: 10.1111/jcmm.17174.
Chen, H., Cui, Y., Zhang, D., Xie, J., & Zhou, X. (2022). The role of fibroblast growth factor 8 in cartilage development and disease. Journal of cellular and molecular medicine, . https://doi.org/10.1111/jcmm.17174
Chen, Haoran, et al. "The role of fibroblast growth factor 8 in cartilage development and disease." Journal of cellular and molecular medicine vol. (2022). doi: https://doi.org/10.1111/jcmm.17174
Chen H, Cui Y, Zhang D, Xie J, Zhou X. The role of fibroblast growth factor 8 in cartilage development and disease. J Cell Mol Med. 2022 Jan 09; doi: 10.1111/jcmm.17174. Epub 2022 Jan 09. PMID: 35001536.
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Predictive and therapeutic implications of a novel PLCγ1/SHP2-driven mechanism of cetuximab resistance in metastatic colorectal cancer.

Clinical cancer research : an official journal of the American Association for Cancer Research

Cruz-Duarte R, de Almeida CR, Negrão M, Fernandes A, Borralho P, Sobral D, Gallego-Paez LM, Machado D, Gramaça J, Vílchez J, Xavier AT, Godinho Ferreira M, Miranda AR, Mansinho H, Brito MJ, Pacheco TR, Abreu C, Lucia-Costa A, Mansinho A, Fior R, Costa L, Martins M.
PMID: 34980600
Clin Cancer Res. 2022 Jan 03; doi: 10.1158/1078-0432.CCR-21-1992. Epub 2022 Jan 03.

PURPOSE: Cetuximab is an epidermal growth factor receptor (EGFR)-targeted therapy approved for the treatment of EXPERIMENTAL DESIGN: We evaluated the value of EGFR effector phospholipase C gamma 1 (PLCγ1) in predicting cetuximab responses, by analyzing progression-free survival (PFS) of...

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Cruz-Duarte R, de Almeida CR, Negrão M, et al. Predictive and therapeutic implications of a novel PLCγ1/SHP2-driven mechanism of cetuximab resistance in metastatic colorectal cancer. Clin Cancer Res. 2022;doi: 10.1158/1078-0432.CCR-21-1992.
Cruz-Duarte, R., de Almeida, C. R., Negrão, M., Fernandes, A., Borralho, P., Sobral, D., Gallego-Paez, L. M., Machado, D., Gramaça, J., Vílchez, J., Xavier, A. T., Godinho Ferreira, M., Miranda, A. R., Mansinho, H., Brito, M. J., Pacheco, T. R., Abreu, C., Lucia-Costa, A., Mansinho, A., Fior, R., Costa, L., & Martins, M. (2022). Predictive and therapeutic implications of a novel PLCγ1/SHP2-driven mechanism of cetuximab resistance in metastatic colorectal cancer. Clinical cancer research : an official journal of the American Association for Cancer Research, . https://doi.org/10.1158/1078-0432.CCR-21-1992
Cruz-Duarte, Raquel, et al. "Predictive and therapeutic implications of a novel PLCγ1/SHP2-driven mechanism of cetuximab resistance in metastatic colorectal cancer." Clinical cancer research : an official journal of the American Association for Cancer Research vol. (2022). doi: https://doi.org/10.1158/1078-0432.CCR-21-1992
Cruz-Duarte R, de Almeida CR, Negrão M, Fernandes A, Borralho P, Sobral D, Gallego-Paez LM, Machado D, Gramaça J, Vílchez J, Xavier AT, Godinho Ferreira M, Miranda AR, Mansinho H, Brito MJ, Pacheco TR, Abreu C, Lucia-Costa A, Mansinho A, Fior R, Costa L, Martins M. Predictive and therapeutic implications of a novel PLCγ1/SHP2-driven mechanism of cetuximab resistance in metastatic colorectal cancer. Clin Cancer Res. 2022 Jan 03; doi: 10.1158/1078-0432.CCR-21-1992. Epub 2022 Jan 03. PMID: 34980600.
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Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates.

Cell communication and signaling : CCS

Caldwell KK, Sosa M, Buckley CT.
PMID: 16445858
Cell Commun Signal. 2006 Jan 30;4:2. doi: 10.1186/1478-811X-4-2.

BACKGROUND: Reversible interactions between the components of cellular signaling pathways allow for the formation and dissociation of multimolecular complexes with spatial and temporal resolution and, thus, are an important means of integrating multiple signals into a coordinated cellular response....

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Caldwell KK, Sosa M, Buckley CT. Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates. Cell Commun Signal. 2006;4:2doi: 10.1186/1478-811X-4-2.
Caldwell, K. K., Sosa, M., & Buckley, C. T. (2006). Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates. Cell communication and signaling : CCS, 42. https://doi.org/10.1186/1478-811X-4-2
Caldwell, Kevin K, et al. "Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates." Cell communication and signaling : CCS vol. 4 (2006): 2. doi: https://doi.org/10.1186/1478-811X-4-2
Caldwell KK, Sosa M, Buckley CT. Identification of mitogen-activated protein kinase docking sites in enzymes that metabolize phosphatidylinositols and inositol phosphates. Cell Commun Signal. 2006 Jan 30;4:2. doi: 10.1186/1478-811X-4-2. PMID: 16445858; PMCID: PMC1379644.
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MrgprX2 regulates mast cell degranulation through PI3K/AKT and PLCγ signaling in pseudo-allergic reactions.

International immunopharmacology

Zhang F, Hong F, Wang L, Fu R, Qi J, Yu B.
PMID: 34920312
Int Immunopharmacol. 2022 Jan;102:108389. doi: 10.1016/j.intimp.2021.108389. Epub 2021 Dec 15.

The G protein-coupled receptor MrgprX2 in mast cells is known to be a crucial receptor for pseudo-allergic reactions. MrgprX2 activation leads to elevated intracellular calcium levels and mast cell degranulation, but the underlying mechanism remains to be elucidated. Herein,...

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Zhang F, Hong F, Wang L, et al. MrgprX2 regulates mast cell degranulation through PI3K/AKT and PLCγ signaling in pseudo-allergic reactions. Int Immunopharmacol. 2021;102:108389doi: 10.1016/j.intimp.2021.108389.
Zhang, F., Hong, F., Wang, L., Fu, R., Qi, J., & Yu, B. (2022). MrgprX2 regulates mast cell degranulation through PI3K/AKT and PLCγ signaling in pseudo-allergic reactions. International immunopharmacology, 102108389. https://doi.org/10.1016/j.intimp.2021.108389
Zhang, Fan, et al. "MrgprX2 regulates mast cell degranulation through PI3K/AKT and PLCγ signaling in pseudo-allergic reactions." International immunopharmacology vol. 102 (2022): 108389. doi: https://doi.org/10.1016/j.intimp.2021.108389
Zhang F, Hong F, Wang L, Fu R, Qi J, Yu B. MrgprX2 regulates mast cell degranulation through PI3K/AKT and PLCγ signaling in pseudo-allergic reactions. Int Immunopharmacol. 2022 Jan;102:108389. doi: 10.1016/j.intimp.2021.108389. Epub 2021 Dec 15. PMID: 34920312.
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Kinomic profiling of glioblastoma cells reveals PLCG1 as a target in restricted glucose.

Biomarker research

Walker K, Boyd NH, Anderson JC, Willey CD, Hjelmeland AB, Meng W.
PMID: 29946469
Biomark Res. 2018 Jun 14;6:22. doi: 10.1186/s40364-018-0136-9. eCollection 2018.

BACKGROUND: For glioblastoma (GBM) treatments to be effective in vivo, understanding the effects of the tumor microenvironment is imperative. In traditional cell culture conditions, glucose concentrations do not model physiologic levels, nor the diminished concentrations found in tumor niches....

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Walker K, Boyd NH, Anderson JC, et al. Kinomic profiling of glioblastoma cells reveals PLCG1 as a target in restricted glucose. Biomark Res. 2018;6:22doi: 10.1186/s40364-018-0136-9.
Walker, K., Boyd, N. H., Anderson, J. C., Willey, C. D., Hjelmeland, A. B., & Meng, W. (2018). Kinomic profiling of glioblastoma cells reveals PLCG1 as a target in restricted glucose. Biomarker research, 622. https://doi.org/10.1186/s40364-018-0136-9
Walker, Kiera, et al. "Kinomic profiling of glioblastoma cells reveals PLCG1 as a target in restricted glucose." Biomarker research vol. 6 (2018): 22. doi: https://doi.org/10.1186/s40364-018-0136-9
Walker K, Boyd NH, Anderson JC, Willey CD, Hjelmeland AB, Meng W. Kinomic profiling of glioblastoma cells reveals PLCG1 as a target in restricted glucose. Biomark Res. 2018 Jun 14;6:22. doi: 10.1186/s40364-018-0136-9. eCollection 2018. PMID: 29946469; PMCID: PMC6001119.
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Intradural cauda equina Candida abscess presenting with hydrocephalus: case report.

Journal of neurosurgery. Spine

Argersinger DP, Natkha VP, Shepard MJ, Thomas AA, Oler AJ, Williamson PR, Chittiboina P, Heiss JD.
PMID: 31470401
J Neurosurg Spine. 2019 Aug 30;1-4. doi: 10.3171/2019.6.SPINE19271. Epub 2019 Aug 30.

Central nervous system (CNS) candida infections are often associated with a poor prognosis. Typically, CNS candidiasis presents as meningitis or microabscesses. Here, the authors report a patient with a challenging presentation of a CNS Candida infection as a discrete,...

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Argersinger DP, Natkha VP, Shepard MJ, et al. Intradural cauda equina Candida abscess presenting with hydrocephalus: case report. J Neurosurg Spine. 2019;1-4doi: 10.3171/2019.6.SPINE19271.
Argersinger, D. P., Natkha, V. P., Shepard, M. J., Thomas, A. A., Oler, A. J., Williamson, P. R., Chittiboina, P., & Heiss, J. D. (2019). Intradural cauda equina Candida abscess presenting with hydrocephalus: case report. Journal of neurosurgery. Spine, 1-4. https://doi.org/10.3171/2019.6.SPINE19271
Argersinger, Davis P, et al. "Intradural cauda equina Candida abscess presenting with hydrocephalus: case report." Journal of neurosurgery. Spine vol. (2019): 1-4. doi: https://doi.org/10.3171/2019.6.SPINE19271
Argersinger DP, Natkha VP, Shepard MJ, Thomas AA, Oler AJ, Williamson PR, Chittiboina P, Heiss JD. Intradural cauda equina Candida abscess presenting with hydrocephalus: case report. J Neurosurg Spine. 2019 Aug 30;1-4. doi: 10.3171/2019.6.SPINE19271. Epub 2019 Aug 30. PMID: 31470401; PMCID: PMC7339489.
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Showing 1 to 12 of 45 entries