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Glycotherapy: A New Paradigm in Breast Cancer Research

Biomolecules (Basel, Switzerland), 2022-03, Vol.12 (4), p.487

2022

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N-acetylglucosaminyl 1-phosphate transferase: an excellent target for developing new generation breast cancer therapeutic

Advances in experimental medicine and biology, 2015-01, Vol.842, p.355

2015

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Dolicholphosphate Mannosyltransferase: A Glycosyltransferase with Unity in Molecular Diversities

The FASEB journal, 2017-04, Vol.31 (S1)

2017

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N‐Glycosylation Inhibitor Interferes with WNT Signaling and Inhibits Angiogenesis

The FASEB journal, 2022-05, Vol.36 (S1), p.n/a

2022

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In Vitro Phosphorylation by cAMP-dependent Protein Kinase Up-regulates Recombinant Saccharomyces cerevisiae Mannosylphosphodolichol Synthase

The Journal of biological chemistry, 2005-02, Vol.280 (6), p.4174-4181

2005

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DPMS is Essential for Tumor Angiogenesis

The FASEB journal, 2019-04, Vol.33 (S1), p.798.2-798.2

2019

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Abstract 444: ER Stress marker GRP78 is not expressed on ER-/PR-/Her2- human breast cancer cell surface or secreted

Cancer research (Chicago, Ill.), 2018-07, Vol.78 (13_Supplement), p.444-444

2018

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Dolichol Phosphate Mannose Synthase: A Glycosyltransferase with Unity in Molecular Diversities

The FASEB journal, 2018-04, Vol.32 (S1), p.544.4-544.4

2018

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Endoplasmic Reticulum (ER) Stress is Anti‐angiogenic and Anti‐tumorigenic

The FASEB journal, 2018-04, Vol.32 (S1), p.544.2-544.2

2018

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ER Stress marker GRP78 is not expressed on ER−/PR−/Her2− human breast cancer cell surface or secreted

The FASEB journal, 2018-04, Vol.32 (S1), p.544.3-544.3

2018

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Unique structural motif supports mannosylphospho dolichol synthase: an important angiogenesis regulator

Current drug targets, 2008-04, Vol.9 (4), p.262-271

2008

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Abstract 4509: GRP78 is neither expressed on ER-/PR-/Her2- human breast cancer cell surface nor secreted in the culture media

Cancer research (Chicago, Ill.), 2017-07, Vol.77 (13_Supplement), p.4509-4509

2017

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Protein N‐glycosylation is an Excellent Target for Developing Novel Breast Cancer Therapeutics

The FASEB journal, 2015-04, Vol.29 (S1)

2015

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GRP78 is Neither Expressed on ER − /PR − /Her2 − Human Breast Cancer Cell Surface nor Secreted

The FASEB journal, 2017-04, Vol.31 (S1)

2017

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Unfolded Protein Response Is Required in nu/nu Mice Microvasculature for Treating Breast Tumor with Tunicamycin

The Journal of biological chemistry, 2011-08, Vol.286 (33), p.29127-29138

2011

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Canonical and non‐canonical pathway of unfolded protein response signaling (607.5)

The FASEB journal, 2014-04, Vol.28 (S1), p.n/a

2014

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GRP78 is Not Expressed on the Surface of Triple Negative Human Breast Cancer Cells

The FASEB journal, 2016-04, Vol.30 (S1)

2016

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Differential gene expression in capillary endothelial cells after inducing unfolded protein response with a protein N‐glycosylation inhibitor

The FASEB journal, 2012-04, Vol.26 (S1)

2012

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Dolichol phosphate mannose synthase: a Glycosyltransferase with Unity in molecular diversities

Glycoconjugate journal, 2017-08, Vol.34 (4), p.467-479

2017

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Tunicamycin-induced ER stress in breast cancer cells neither expresses GRP78 on the surface nor secretes it into the media

Glycobiology (Oxford), 2018-02, Vol.28 (2), p.61-68

2018

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Abstract 1243: Therapeutic ER stress induced by tunicamycin is anti-angiogenic/anti-tumorigenic and signals through unfolded protein response

Cancer research (Chicago, Ill.), 2015-08, Vol.75 (15_Supplement), p.1243-1243

2015

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Abstract 2865: Dual action glycotherapy for triple negative breast cancer

Cancer research (Chicago, Ill.), 2016-07, Vol.76 (14_Supplement), p.2865-2865

2016

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Nano‐formulation Enhances the Anti‐angiogenic Potential of Tunicamycin

The FASEB journal, 2015-04, Vol.29 (S1)

2015

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Upregulated Expression of GRP78 Supports ER Stress‐induced Apoptosis in Tunicamycin Treated Triple Negative Breast Tumor

The FASEB journal, 2016-04, Vol.30 (S1)

2016

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Genome‐wide expression profiling in capillary endothelial cells following Tunicamycin‐induced unfolded protein response

The FASEB journal, 2011-04, Vol.25 (S1), p.964.1-964.1

2011

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Glycotherapy: A New Paradigm in Breast Cancer Research

N-acetylglucosaminyl 1-phosphate transferase: an excellent target for developing new generation breast cancer therapeutic

Dolicholphosphate Mannosyltransferase: A Glycosyltransferase with Unity in Molecular Diversities

N‐Glycosylation Inhibitor Interferes with WNT Signaling and Inhibits Angiogenesis

In Vitro Phosphorylation by cAMP-dependent Protein Kinase Up-regulates Recombinant Saccharomyces cerevisiae Mannosylphosphodolichol Synthase

DPMS is Essential for Tumor Angiogenesis

Abstract 444: ER Stress marker GRP78 is not expressed on ER-/PR-/Her2- human breast cancer cell surface or secreted

Dolichol Phosphate Mannose Synthase: A Glycosyltransferase with Unity in Molecular Diversities

Endoplasmic Reticulum (ER) Stress is Anti‐angiogenic and Anti‐tumorigenic

ER Stress marker GRP78 is not expressed on ER−/PR−/Her2− human breast cancer cell surface or secreted

Unique structural motif supports mannosylphospho dolichol synthase: an important angiogenesis regulator

Abstract 4509: GRP78 is neither expressed on ER-/PR-/Her2- human breast cancer cell surface nor secreted in the culture media

Protein N‐glycosylation is an Excellent Target for Developing Novel Breast Cancer Therapeutics

GRP78 is Neither Expressed on ER − /PR − /Her2 − Human Breast Cancer Cell Surface nor Secreted

Unfolded Protein Response Is Required in nu/nu Mice Microvasculature for Treating Breast Tumor with Tunicamycin

Canonical and non‐canonical pathway of unfolded protein response signaling (607.5)

GRP78 is Not Expressed on the Surface of Triple Negative Human Breast Cancer Cells

Differential gene expression in capillary endothelial cells after inducing unfolded protein response with a protein N‐glycosylation inhibitor

Dolichol phosphate mannose synthase: a Glycosyltransferase with Unity in molecular diversities

Tunicamycin-induced ER stress in breast cancer cells neither expresses GRP78 on the surface nor secretes it into the media

Abstract 1243: Therapeutic ER stress induced by tunicamycin is anti-angiogenic/anti-tumorigenic and signals through unfolded protein response

Abstract 2865: Dual action glycotherapy for triple negative breast cancer

Nano‐formulation Enhances the Anti‐angiogenic Potential of Tunicamycin

Upregulated Expression of GRP78 Supports ER Stress‐induced Apoptosis in Tunicamycin Treated Triple Negative Breast Tumor

Genome‐wide expression profiling in capillary endothelial cells following Tunicamycin‐induced unfolded protein response

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