Avid Bioservices Inc (CDMO)

[biopharm]

JNCJ, many believe in PS Targeting and as the facts come in, it will be sound science and a disturbance to Big Pharma? Hell yes

I will pick out just one of the MANY that can't deny it anymore and you also think Univ of Texas Board of Regents is aware? YES

John F Hancock knows well how astronomical PS Targeting is right now

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PS Targeting patent filed when they did not realize lol that it was PS Targeting / ...but look, 3 years later they publish research saying clearly it is PS Targeting ... so we see the bias from Board of Regents Univ of Texas System and clear conflicts of interest from Board of Regents - Univ of Texas System

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Methods and compositions for use with K-ras mediated disorders
Patent number: 9474730
Abstract: Methods and compositions that can be used to identify and characterize inhibitors of K-ras localization to the plasma membrane and in doing so inhibit the signal transduction of K-ras. Such compositions can be used to treat K-ras mediated disorders, such as cancer.
Type: Grant
Filed: April 30, 2013
Date of Patent: October 25, 2016
Assignee: BOARD OF REGENTS OF THE UNIVERSITY OF TEXAS SYSTEM

Inventors: John F. Hancock, Dharini Van Der Hoeven, Kwang-Jin Cho


https://patents.justia.com/inventor/dharini-van-der-hoeven

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Targeting plasma membrane phosphatidylserine content to inhibit oncogenic KRAS function

Article (PDF Available) ·
October 2019 with 51 Reads

Walaa Kattan at University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences

Walaa Kattan
University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences

Wei Chen

Xiaoping Ma

Tien Hung Lan

Dharini van der Hoeven

Ransome van der Hoeven

John F Hancock

Abstract
The small GTPase KRAS, which is frequently mutated in human cancers, must be localized to the plasma membrane (PM) for biological activity. We recently showed that the KRAS C-terminal membrane anchor exhibits exquisite lipid-binding specificity for select species of phosphatidylserine (PtdSer). We, therefore, investigated whether reducing PM PtdSer content is sufficient to abrogate KRAS oncogenesis. Oxysterol-related binding proteins ORP5 and ORP8 exchange PtdSer synthesized in the ER for phosphatidyl-4-phosphate synthesized in the PM. We show that depletion of ORP5 or ORP8 reduced PM PtdSer levels, resulting in extensive mislocalization of KRAS from the PM. Concordantly, ORP5 or ORP8 depletion significantly reduced proliferation and anchorage-independent growth of multiple KRAS-dependent cancer cell lines, and attenuated KRAS signaling in vivo. Similarly, functionally inhibiting ORP5 and ORP8 by inhibiting PI4KIIIα-mediated synthesis of phosphatidyl-4-phosphate at the PM selectively inhibited the growth of KRAS-dependent cancer cell lines over normal cells. Inhibiting KRAS function through regulating PM lipid PtdSer content may represent a viable strategy for KRAS-driven cancers.

https://www.researchgate.net/publication/335416493_Targeting_plasma_membrane_phosphatidylserine_content_to_inhibit_oncogenic_KRAS_function/fulltext/5d648dc392851c619d781a44/335416493_Targeting_plasma_membrane_phosphatidylserine_content_to_inhibit_oncogenic_KRAS_function.pdf?origin=publication_detail