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Tumor suppressor Par-4 = structural ...
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Rangnekar, Vivek.
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Tumor suppressor Par-4 = structural features, molecular mechanisms and function /
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Tumor suppressor Par-4/ edited by Vivek M. Rangnekar.
其他題名:
structural features, molecular mechanisms and function /
其他作者:
Rangnekar, Vivek.
出版者:
Cham :Springer International Publishing : : 2022.,
面頁冊數:
x, 323 p. :ill. (chiefly col.), digital ;24 cm.
內容註:
Discovery and Overview of Par-4 -- Par-4 in cell cycle regulation -- Conformational studies of the Par-4 C-terminal Domain -- Structural analysis of Par-4 and crystallographic analysis of the regulatory domain -- Regulation of Par-4 by Ubiquitinases -- REGULATION OF PAR-4 FUNCTION BY PHOSPHORYLATION -- Role of Par-4 in GRP78 translocation -- PAR-4 in the regulation of stem cell death and embryo development -- RASSF2 and the PAR-4 connection -- Regulation of tumor suppressor Par-4 by ceramide -- PAWR as a direct SRC-1/HOXC11 suppression target -- Index.
Contained By:
Springer Nature eBook
標題:
Tumor suppressor proteins. -
電子資源:
https://doi.org/10.1007/978-3-030-73572-2
ISBN:
9783030735722
Tumor suppressor Par-4 = structural features, molecular mechanisms and function /
Tumor suppressor Par-4
structural features, molecular mechanisms and function /[electronic resource] :edited by Vivek M. Rangnekar. - Cham :Springer International Publishing :2022. - x, 323 p. :ill. (chiefly col.), digital ;24 cm.
Discovery and Overview of Par-4 -- Par-4 in cell cycle regulation -- Conformational studies of the Par-4 C-terminal Domain -- Structural analysis of Par-4 and crystallographic analysis of the regulatory domain -- Regulation of Par-4 by Ubiquitinases -- REGULATION OF PAR-4 FUNCTION BY PHOSPHORYLATION -- Role of Par-4 in GRP78 translocation -- PAR-4 in the regulation of stem cell death and embryo development -- RASSF2 and the PAR-4 connection -- Regulation of tumor suppressor Par-4 by ceramide -- PAWR as a direct SRC-1/HOXC11 suppression target -- Index.
Par-4 is a tumor suppressor protein first discovered and identified in 1993 by Dr. Vivek Rangnekar's laboratory in prostate cancer cells undergoing apoptosis. Par-4 (later also known as PAWR) is a naturally occurring tumor suppressor. Studies have indicated that Par-4 selectively induces apoptosis in cancer cells while leaving normal, healthy, cells unaffected. Mechanisms contributing to the cancer-selective action of Par-4 have been associated with protein kinase A activation of intracellular Par-4 in cancer cells or GRP78 expression primarily on the surface of cancer cells. Par-4 is downregulated, inactivated or mutated in diverse cancers. This first of two volumes will be the first on the market on the topic of Par-4, and will provide the opportunity for researchers to discuss the future direction of studies, broaden the scope of research, and contribute a more complete understanding of the molecule's structural features, key functional domains, regulation and relevant basic and clinical/translational facets.
ISBN: 9783030735722
Standard No.: 10.1007/978-3-030-73572-2doiSubjects--Topical Terms:
1243843
Tumor suppressor proteins.
LC Class. No.: QR188.6 / .T86 2022
Dewey Class. No.: 612.01575
Tumor suppressor Par-4 = structural features, molecular mechanisms and function /
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Discovery and Overview of Par-4 -- Par-4 in cell cycle regulation -- Conformational studies of the Par-4 C-terminal Domain -- Structural analysis of Par-4 and crystallographic analysis of the regulatory domain -- Regulation of Par-4 by Ubiquitinases -- REGULATION OF PAR-4 FUNCTION BY PHOSPHORYLATION -- Role of Par-4 in GRP78 translocation -- PAR-4 in the regulation of stem cell death and embryo development -- RASSF2 and the PAR-4 connection -- Regulation of tumor suppressor Par-4 by ceramide -- PAWR as a direct SRC-1/HOXC11 suppression target -- Index.
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Par-4 is a tumor suppressor protein first discovered and identified in 1993 by Dr. Vivek Rangnekar's laboratory in prostate cancer cells undergoing apoptosis. Par-4 (later also known as PAWR) is a naturally occurring tumor suppressor. Studies have indicated that Par-4 selectively induces apoptosis in cancer cells while leaving normal, healthy, cells unaffected. Mechanisms contributing to the cancer-selective action of Par-4 have been associated with protein kinase A activation of intracellular Par-4 in cancer cells or GRP78 expression primarily on the surface of cancer cells. Par-4 is downregulated, inactivated or mutated in diverse cancers. This first of two volumes will be the first on the market on the topic of Par-4, and will provide the opportunity for researchers to discuss the future direction of studies, broaden the scope of research, and contribute a more complete understanding of the molecule's structural features, key functional domains, regulation and relevant basic and clinical/translational facets.
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