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Showing 13 to 24 of 45 entries
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Mycosis Fungoides and Sézary Syndrome: An Integrative Review of the Pathophysiology, Molecular Drivers, and Targeted Therapy.

Cancers

García-Díaz N, Piris MÁ, Ortiz-Romero PL, Vaqué JP.
PMID: 33923722
Cancers (Basel). 2021 Apr 16;13(8). doi: 10.3390/cancers13081931.

Primary cutaneous T-cell lymphomas (CTCLs) constitute a heterogeneous group of diseases that affect the skin. Mycosis fungoides (MF) and Sézary syndrome (SS) account for the majority of these lesions and have recently been the focus of extensive translational research....

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García-Díaz N, Piris MÁ, Ortiz-Romero PL, et al. Mycosis Fungoides and Sézary Syndrome: An Integrative Review of the Pathophysiology, Molecular Drivers, and Targeted Therapy. Cancers (Basel). 2021;13(8)doi: 10.3390/cancers13081931.
García-Díaz, N., Piris, M. �. �., Ortiz-Romero, P. L., & Vaqué, J. P. (2021). Mycosis Fungoides and Sézary Syndrome: An Integrative Review of the Pathophysiology, Molecular Drivers, and Targeted Therapy. Cancers, 13(8), . https://doi.org/10.3390/cancers13081931
García-Díaz, Nuria, et al. "Mycosis Fungoides and Sézary Syndrome: An Integrative Review of the Pathophysiology, Molecular Drivers, and Targeted Therapy." Cancers vol. 13,8 (2021). doi: https://doi.org/10.3390/cancers13081931
García-Díaz N, Piris MÁ, Ortiz-Romero PL, Vaqué JP. Mycosis Fungoides and Sézary Syndrome: An Integrative Review of the Pathophysiology, Molecular Drivers, and Targeted Therapy. Cancers (Basel). 2021 Apr 16;13(8). doi: 10.3390/cancers13081931. PMID: 33923722; PMCID: PMC8074086.
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NAD.

Cell reports

Wang Y, Wang F, Wang L, Qiu S, Yao Y, Yan C, Xiong X, Chen X, Ji Q, Cao J, Gao G, Li D, Zhang L, Guo Z, Wang R, Wang H, Fan G.
PMID: 34380043
Cell Rep. 2021 Aug 10;36(6):109516. doi: 10.1016/j.celrep.2021.109516.

Although tumor-infiltrating lymphocytes (TILs) maintain their ability to proliferate, persist, and eradicate tumors, they are frequently dysfunctional in situ. By performing both whole-genome CRISPR and metabolic inhibitor screens, we identify that nicotinamide phosphoribosyltransferase (NAMPT) is required for T cell...

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Wang Y, Wang F, Wang L, et al. NAD. Cell Rep. 2021;36(6):109516doi: 10.1016/j.celrep.2021.109516.
Wang, Y., Wang, F., Wang, L., Qiu, S., Yao, Y., Yan, C., Xiong, X., Chen, X., Ji, Q., Cao, J., Gao, G., Li, D., Zhang, L., Guo, Z., Wang, R., Wang, H., & Fan, G. (2021). NAD. Cell reports, 36(6), 109516. https://doi.org/10.1016/j.celrep.2021.109516
Wang, Yuetong, et al. "NAD." Cell reports vol. 36,6 (2021): 109516. doi: https://doi.org/10.1016/j.celrep.2021.109516
Wang Y, Wang F, Wang L, Qiu S, Yao Y, Yan C, Xiong X, Chen X, Ji Q, Cao J, Gao G, Li D, Zhang L, Guo Z, Wang R, Wang H, Fan G. NAD. Cell Rep. 2021 Aug 10;36(6):109516. doi: 10.1016/j.celrep.2021.109516. PMID: 34380043.
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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...

Cite
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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The Role of Fibroblast Growth Factor (FGF) Signaling in Tissue Repair and Regeneration.

Cells

Farooq M, Khan AW, Kim MS, Choi S.
PMID: 34831463
Cells. 2021 Nov 19;10(11). doi: 10.3390/cells10113242.

Fibroblast growth factors (FGFs) are a large family of secretory molecules that act through tyrosine kinase receptors known as FGF receptors. They play crucial roles in a wide variety of cellular functions, including cell proliferation, survival, metabolism, morphogenesis, and...

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Farooq M, Khan AW, Kim MS, et al. The Role of Fibroblast Growth Factor (FGF) Signaling in Tissue Repair and Regeneration. Cells. 2021;10(11)doi: 10.3390/cells10113242.
Farooq, M., Khan, A. W., Kim, M. S., & Choi, S. (2021). The Role of Fibroblast Growth Factor (FGF) Signaling in Tissue Repair and Regeneration. Cells, 10(11), . https://doi.org/10.3390/cells10113242
Farooq, Mariya, et al. "The Role of Fibroblast Growth Factor (FGF) Signaling in Tissue Repair and Regeneration." Cells vol. 10,11 (2021). doi: https://doi.org/10.3390/cells10113242
Farooq M, Khan AW, Kim MS, Choi S. The Role of Fibroblast Growth Factor (FGF) Signaling in Tissue Repair and Regeneration. Cells. 2021 Nov 19;10(11). doi: 10.3390/cells10113242. PMID: 34831463; PMCID: PMC8622657.
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NAD.

Cell reports

Wang Y, Wang F, Wang L, Qiu S, Yao Y, Yan C, Xiong X, Chen X, Ji Q, Cao J, Gao G, Li D, Zhang L, Guo Z, Wang R, Wang H, Fan G.
PMID: 34380043
Cell Rep. 2021 Aug 10;36(6):109516. doi: 10.1016/j.celrep.2021.109516.

Although tumor-infiltrating lymphocytes (TILs) maintain their ability to proliferate, persist, and eradicate tumors, they are frequently dysfunctional in situ. By performing both whole-genome CRISPR and metabolic inhibitor screens, we identify that nicotinamide phosphoribosyltransferase (NAMPT) is required for T cell...

Cite
Wang Y, Wang F, Wang L, et al. NAD. Cell Rep. 2021;36(6):109516doi: 10.1016/j.celrep.2021.109516.
Wang, Y., Wang, F., Wang, L., Qiu, S., Yao, Y., Yan, C., Xiong, X., Chen, X., Ji, Q., Cao, J., Gao, G., Li, D., Zhang, L., Guo, Z., Wang, R., Wang, H., & Fan, G. (2021). NAD. Cell reports, 36(6), 109516. https://doi.org/10.1016/j.celrep.2021.109516
Wang, Yuetong, et al. "NAD." Cell reports vol. 36,6 (2021): 109516. doi: https://doi.org/10.1016/j.celrep.2021.109516
Wang Y, Wang F, Wang L, Qiu S, Yao Y, Yan C, Xiong X, Chen X, Ji Q, Cao J, Gao G, Li D, Zhang L, Guo Z, Wang R, Wang H, Fan G. NAD. Cell Rep. 2021 Aug 10;36(6):109516. doi: 10.1016/j.celrep.2021.109516. PMID: 34380043.
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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...

Cite
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...

Cite
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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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...

Cite
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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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. 2021 Dec 14;102:108389. doi: 10.1016/j.intimp.2021.108389. Epub 2021 Dec 14.

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,...

Cite
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. (2021). 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 (2021): 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. 2021 Dec 14;102:108389. doi: 10.1016/j.intimp.2021.108389. Epub 2021 Dec 14. PMID: 34920312.
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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...

Cite
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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Up-regulation of Phosphatidylinositol-3 Kinase Signaling in plcg1 Gene Null Fibroblasts.

Sheng wu hua xue yu sheng wu wu li xue bao Acta biochimica et biophysica Sinica

Bai XC, Luo SQ, Bai J, Deng F, Zheng WS, Ji QS.
PMID: 12035061
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai). 2001;33(6):677-681.

Phospholipase C-gamma1(PLC-gamma1) and phosphatidylinositol-3 kinase(PI-3K) play crucial role in growth factor-induced cell growth and proliferation. To investigate the complementary mechanism of PLC-gamma1 in cell growth and epidermal growth factor (EGF)-induced mitogenic signaling, PLC-gamma1 deficient mouse embryonic fibroblasts(PLC-gamma1(-/-)) and its...

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Bai XC, Luo SQ, Bai J, et al. Up-regulation of Phosphatidylinositol-3 Kinase Signaling in plcg1 Gene Null Fibroblasts. Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai). 2001;33(6):677-681
Bai, X. C., Luo, S. Q., Bai, J., Deng, F., Zheng, W. S., & Ji, Q. S. (2001). Up-regulation of Phosphatidylinositol-3 Kinase Signaling in plcg1 Gene Null Fibroblasts. Sheng wu hua xue yu sheng wu wu li xue bao Acta biochimica et biophysica Sinica, 33(6), 677-681.
Bai, X C, et al. "Up-regulation of Phosphatidylinositol-3 Kinase Signaling in plcg1 Gene Null Fibroblasts." Sheng wu hua xue yu sheng wu wu li xue bao Acta biochimica et biophysica Sinica vol. 33,6 (2001): 677-681.
Bai XC, Luo SQ, Bai J, Deng F, Zheng WS, Ji QS. Up-regulation of Phosphatidylinositol-3 Kinase Signaling in plcg1 Gene Null Fibroblasts. Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai). 2001;33(6):677-681. PMID: 12035061.
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Expression of phospholipase-gamma1 in human fetal tissues.

Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA

Hou YX, Luo SQ, Ji QS.
PMID: 12426156
Di Yi Jun Yi Da Xue Xue Bao. 2001;21(12):888-889.

OBJECTIVE: To investigate the expression of phospholipase C-gamma1(PLC-gamma1) in human fetal tissues. METHODS: Serial sections 5 &mgr;m in thickness were prepared from paraformadehyde-fixed and paraffin-embedded normal human fetal tissues including the cartilage, the cartilage membrane and the muscle tissues....

Cite
Hou YX, Luo SQ, Ji QS. Expression of phospholipase-gamma1 in human fetal tissues. Di Yi Jun Yi Da Xue Xue Bao. 2001;21(12):888-889
Hou, Y. X., Luo, S. Q., & Ji, Q. S. (2001). Expression of phospholipase-gamma1 in human fetal tissues. Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA, 21(12), 888-889.
Hou, Yun-Xia, et al. "Expression of phospholipase-gamma1 in human fetal tissues." Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA vol. 21,12 (2001): 888-889.
Hou YX, Luo SQ, Ji QS. Expression of phospholipase-gamma1 in human fetal tissues. Di Yi Jun Yi Da Xue Xue Bao. 2001;21(12):888-889. PMID: 12426156.
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Showing 13 to 24 of 45 entries