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Showing 1 to 8 of 8 entries
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The matrix protein Fibulin-3 promotes KISS1R induced triple negative breast cancer cell invasion.

Oncotarget

Noonan MM, Dragan M, Mehta MM, Hess DA, Brackstone M, Tuck AB, Viswakarma N, Rana A, Babwah AV, Wondisford FE, Bhattacharya M.
PMID: 30046386
Oncotarget. 2018 Jul 10;9(53):30034-30052. doi: 10.18632/oncotarget.25682. eCollection 2018 Jul 10.

Breast cancer is a leading cause of cancer mortality. In particular, triple negative breast cancer (TNBC) comprise a heterogeneous group of basal-like tumors lacking estrogen receptor (ERĪ±), progesterone receptor (PR) and HER2 (ErbB2). TNBC represents 15-20% of all breast...

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Noonan MM, Dragan M, Mehta MM, et al. The matrix protein Fibulin-3 promotes KISS1R induced triple negative breast cancer cell invasion. Oncotarget. 2018;9(53):30034-30052doi: 10.18632/oncotarget.25682.
Noonan, M. M., Dragan, M., Mehta, M. M., Hess, D. A., Brackstone, M., Tuck, A. B., Viswakarma, N., Rana, A., Babwah, A. V., Wondisford, F. E., & Bhattacharya, M. (2018). The matrix protein Fibulin-3 promotes KISS1R induced triple negative breast cancer cell invasion. Oncotarget, 9(53), 30034-30052. https://doi.org/10.18632/oncotarget.25682
Noonan, Michelle M, et al. "The matrix protein Fibulin-3 promotes KISS1R induced triple negative breast cancer cell invasion." Oncotarget vol. 9,53 (2018): 30034-30052. doi: https://doi.org/10.18632/oncotarget.25682
Noonan MM, Dragan M, Mehta MM, Hess DA, Brackstone M, Tuck AB, Viswakarma N, Rana A, Babwah AV, Wondisford FE, Bhattacharya M. The matrix protein Fibulin-3 promotes KISS1R induced triple negative breast cancer cell invasion. Oncotarget. 2018 Jul 10;9(53):30034-30052. doi: 10.18632/oncotarget.25682. eCollection 2018 Jul 10. PMID: 30046386; PMCID: PMC6059025.
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Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays.

Cells

Gamboa CM, Wang Y, Xu H, Kalemba K, Wondisford FE, Sabaawy HE.
PMID: 34943788
Cells. 2021 Nov 24;10(12). doi: 10.3390/cells10123280.

The liver is among the principal organs for glucose homeostasis and metabolism. Studies of liver metabolism are limited by the inability to expand primary hepatocytes in vitro while maintaining their metabolic functions. Human hepatic three-dimensional (3D) organoids have been...

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Gamboa CM, Wang Y, Xu H, et al. Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays. Cells. 2021;10(12)doi: 10.3390/cells10123280.
Gamboa, C. M., Wang, Y., Xu, H., Kalemba, K., Wondisford, F. E., & Sabaawy, H. E. (2021). Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays. Cells, 10(12), . https://doi.org/10.3390/cells10123280
Gamboa, Christian Moya, et al. "Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays." Cells vol. 10,12 (2021). doi: https://doi.org/10.3390/cells10123280
Gamboa CM, Wang Y, Xu H, Kalemba K, Wondisford FE, Sabaawy HE. Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays. Cells. 2021 Nov 24;10(12). doi: 10.3390/cells10123280. PMID: 34943788.
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Familial Congenital Hypothyroidism Caused by Abnormal and Bioinactive TSH due to Mutations in the beta-Subunit Gene.

Trends in endocrinology and metabolism: TEM

Medeiros-Neto G, de Lacerda L, Wondisford FE.
PMID: 18406781
Trends Endocrinol Metab. 1997 Jan-Feb;8(1):15-20. doi: 10.1016/s1043-2760(96)00203-2.

Hereditary TSH deficiency is a rare autosomal recessive disease described in inbred Japanese families and in Greek and Brazilian kindreds. The TSH-beta-subunit gene has been shown to be the site of mutations that will give rise to truncated proteins...

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Medeiros-Neto G, de Lacerda L, Wondisford FE. Familial Congenital Hypothyroidism Caused by Abnormal and Bioinactive TSH due to Mutations in the beta-Subunit Gene. Trends Endocrinol Metab. 1997;8(1):15-20doi: 10.1016/s1043-2760(96)00203-2.
Medeiros-Neto, G., de Lacerda, L., & Wondisford, F. E. (1997). Familial Congenital Hypothyroidism Caused by Abnormal and Bioinactive TSH due to Mutations in the beta-Subunit Gene. Trends in endocrinology and metabolism: TEM, 8(1), 15-20. https://doi.org/10.1016/s1043-2760(96)00203-2
Medeiros-Neto, G, et al. "Familial Congenital Hypothyroidism Caused by Abnormal and Bioinactive TSH due to Mutations in the beta-Subunit Gene." Trends in endocrinology and metabolism: TEM vol. 8,1 (1997): 15-20. doi: https://doi.org/10.1016/s1043-2760(96)00203-2
Medeiros-Neto G, de Lacerda L, Wondisford FE. Familial Congenital Hypothyroidism Caused by Abnormal and Bioinactive TSH due to Mutations in the beta-Subunit Gene. Trends Endocrinol Metab. 1997 Jan-Feb;8(1):15-20. doi: 10.1016/s1043-2760(96)00203-2. PMID: 18406781.
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Transcription Factors and Hypopituitarism.

Trends in endocrinology and metabolism: TEM

Cohen LE, Radovick S, Wondisford FE.
PMID: 10481164
Trends Endocrinol Metab. 1999 Oct;10(8):326-332. doi: 10.1016/s1043-2760(99)00180-0.

Several homeodomain factors are found in the developing anterior pituitary lobe. The production of these developmental transcription factors has distinct temporal and spatial patterns. By interacting with each other, as well as with other extrinsic and intrinsic signals, they...

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Cohen LE, Radovick S, Wondisford FE. Transcription Factors and Hypopituitarism. Trends Endocrinol Metab. 1999;10(8):326-332doi: 10.1016/s1043-2760(99)00180-0.
Cohen, L. E., Radovick, S., & Wondisford, F. E. (1999). Transcription Factors and Hypopituitarism. Trends in endocrinology and metabolism: TEM, 10(8), 326-332. https://doi.org/10.1016/s1043-2760(99)00180-0
Cohen, et al. "Transcription Factors and Hypopituitarism." Trends in endocrinology and metabolism: TEM vol. 10,8 (1999): 326-332. doi: https://doi.org/10.1016/s1043-2760(99)00180-0
Cohen LE, Radovick S, Wondisford FE. Transcription Factors and Hypopituitarism. Trends Endocrinol Metab. 1999 Oct;10(8):326-332. doi: 10.1016/s1043-2760(99)00180-0. PMID: 10481164.
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Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays.

Cells

Gamboa CM, Wang Y, Xu H, Kalemba K, Wondisford FE, Sabaawy HE.
PMID: 34943788
Cells. 2021 Nov 24;10(12). doi: 10.3390/cells10123280.

The liver is among the principal organs for glucose homeostasis and metabolism. Studies of liver metabolism are limited by the inability to expand primary hepatocytes in vitro while maintaining their metabolic functions. Human hepatic three-dimensional (3D) organoids have been...

Cite
Gamboa CM, Wang Y, Xu H, et al. Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays. Cells. 2021;10(12)doi: 10.3390/cells10123280.
Gamboa, C. M., Wang, Y., Xu, H., Kalemba, K., Wondisford, F. E., & Sabaawy, H. E. (2021). Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays. Cells, 10(12), . https://doi.org/10.3390/cells10123280
Gamboa, Christian Moya, et al. "Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays." Cells vol. 10,12 (2021). doi: https://doi.org/10.3390/cells10123280
Gamboa CM, Wang Y, Xu H, Kalemba K, Wondisford FE, Sabaawy HE. Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays. Cells. 2021 Nov 24;10(12). doi: 10.3390/cells10123280. PMID: 34943788; PMCID: PMC8699701.
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Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays.

Cells

Gamboa CM, Wang Y, Xu H, Kalemba K, Wondisford FE, Sabaawy HE.
PMID: 34943788
Cells. 2021 Nov 24;10(12). doi: 10.3390/cells10123280.

The liver is among the principal organs for glucose homeostasis and metabolism. Studies of liver metabolism are limited by the inability to expand primary hepatocytes in vitro while maintaining their metabolic functions. Human hepatic three-dimensional (3D) organoids have been...

Cite
Gamboa CM, Wang Y, Xu H, et al. Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays. Cells. 2021;10(12)doi: 10.3390/cells10123280.
Gamboa, C. M., Wang, Y., Xu, H., Kalemba, K., Wondisford, F. E., & Sabaawy, H. E. (2021). Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays. Cells, 10(12), . https://doi.org/10.3390/cells10123280
Gamboa, Christian Moya, et al. "Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays." Cells vol. 10,12 (2021). doi: https://doi.org/10.3390/cells10123280
Gamboa CM, Wang Y, Xu H, Kalemba K, Wondisford FE, Sabaawy HE. Optimized 3D Culture of Hepatic Cells for Liver Organoid Metabolic Assays. Cells. 2021 Nov 24;10(12). doi: 10.3390/cells10123280. PMID: 34943788; PMCID: PMC8699701.
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Metabolic Flux Analysis-Linking Isotope Labeling and Metabolic Fluxes.

Metabolites

Wang Y, Wondisford FE, Song C, Zhang T, Su X.
PMID: 33172051
Metabolites. 2020 Nov 06;10(11). doi: 10.3390/metabo10110447.

Metabolic flux analysis (MFA) is an increasingly important tool to study metabolism quantitatively. Unlike the concentrations of metabolites, the fluxes, which are the rates at which intracellular metabolites interconvert, are not directly measurable. MFA uses stable isotope labeled tracers...

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Wang Y, Wondisford FE, Song C, et al. Metabolic Flux Analysis-Linking Isotope Labeling and Metabolic Fluxes. Metabolites. 2020;10(11)doi: 10.3390/metabo10110447.
Wang, Y., Wondisford, F. E., Song, C., Zhang, T., & Su, X. (2020). Metabolic Flux Analysis-Linking Isotope Labeling and Metabolic Fluxes. Metabolites, 10(11), . https://doi.org/10.3390/metabo10110447
Wang, Yujue, et al. "Metabolic Flux Analysis-Linking Isotope Labeling and Metabolic Fluxes." Metabolites vol. 10,11 (2020). doi: https://doi.org/10.3390/metabo10110447
Wang Y, Wondisford FE, Song C, Zhang T, Su X. Metabolic Flux Analysis-Linking Isotope Labeling and Metabolic Fluxes. Metabolites. 2020 Nov 06;10(11). doi: 10.3390/metabo10110447. PMID: 33172051; PMCID: PMC7694648.
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Hyperglucagonemia Mitigates the Effect of Metformin on Glucose Production in Prediabetes.

Cell reports

Konopka AR, Esponda RR, Robinson MM, Johnson ML, Carter RE, Schiavon M, Cobelli C, Wondisford FE, Lanza IR, Nair KS.
PMID: 29791861
Cell Rep. 2018 May 22;23(8):2532. doi: 10.1016/j.celrep.2018.05.027.

No abstract available.

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Konopka AR, Esponda RR, Robinson MM, et al. Hyperglucagonemia Mitigates the Effect of Metformin on Glucose Production in Prediabetes. Cell Rep. 2018;23(8):2532doi: 10.1016/j.celrep.2018.05.027.
Konopka, A. R., Esponda, R. R., Robinson, M. M., Johnson, M. L., Carter, R. E., Schiavon, M., Cobelli, C., Wondisford, F. E., Lanza, I. R., & Nair, K. S. (2018). Hyperglucagonemia Mitigates the Effect of Metformin on Glucose Production in Prediabetes. Cell reports, 23(8), 2532. https://doi.org/10.1016/j.celrep.2018.05.027
Konopka, Adam R, et al. "Hyperglucagonemia Mitigates the Effect of Metformin on Glucose Production in Prediabetes." Cell reports vol. 23,8 (2018): 2532. doi: https://doi.org/10.1016/j.celrep.2018.05.027
Konopka AR, Esponda RR, Robinson MM, Johnson ML, Carter RE, Schiavon M, Cobelli C, Wondisford FE, Lanza IR, Nair KS. Hyperglucagonemia Mitigates the Effect of Metformin on Glucose Production in Prediabetes. Cell Rep. 2018 May 22;23(8):2532. doi: 10.1016/j.celrep.2018.05.027. PMID: 29791861; PMCID: PMC6143136.
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Showing 1 to 8 of 8 entries