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Vector Winter 2016 [PDF]

open access: yes, 2016
Vector is the student engineering magazine on campus. Published by the Student Engineering Council, Vector is completely written, managed, and designed by students for students.
University of Texas at Austin
core   +1 more source

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

open access: yesMolecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu   +13 more
wiley   +1 more source

CEACAM1 participation in breast cancer progression

open access: yesMolecular Oncology, EarlyView.
In invasive breast cancer (BC), CEACAM1 shifts from an apical to a uniform membranous/cytoplasmic pattern, or is lost, as tumors dedifferentiate, inversely tracking the Ki‐67 proliferative index. In MCF‐7 cells, only CEACAM1‐4L suppresses proliferation, repressing cell cycle and growth factor genes.
Mykola Lyndin   +3 more
wiley   +1 more source

Vector Fall 2011 [PDF]

open access: yes, 2011
Vector is the student engineering magazine on campus. Published by the Student Engineering Council, Vector is completely written, managed, and designed by students for students.
University of Texas at Austin
core   +1 more source

Partial FAK suppression promotes tumor growth, an effect reversed by macrophage p110δ PI3K inactivation

open access: yesMolecular Oncology, EarlyView.
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou   +4 more
wiley   +1 more source

Vector Summer 2016 [PDF]

open access: yes, 2016
Vector is the student engineering magazine on campus. Published by the Student Engineering Council, Vector is completely written, managed, and designed by students for students.
University of Texas at Austin
core   +1 more source

NAPRT loss promotes lung tumor initiation and growth through AKT signaling independently of NAD+ biosynthesis

open access: yesMolecular Oncology, EarlyView.
Loss of NAPRT promotes lung tumor initiation and growth through a noncanonical mechanism, independent of its role in NAD+ biosynthesis. Mechanistically, NAPRT depletion activates the mTORC2‐driven AKT/β‐catenin signaling axis to enhance clonogenic and invasive phenotypes. Furthermore, lung‐specific Naprt deletion significantly increases tumor burden in
Myung Joon Oh   +11 more
wiley   +1 more source

Nationwide cross-sectional surveillance of Leishmania donovani in phlebotomine sand flies and its impact on national kala-azar elimination in India

open access: yesScientific Reports
India is accelerating efforts to eliminate kala-azar by aligning its National Kala-Azar Elimination Program with the World Health Organization’s (WHO) roadmap for Neglected Tropical Diseases (NTDs) 2021–2030.
Harish Kumar Shah   +11 more
doaj   +1 more source

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

open access: yesMolecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim   +11 more
wiley   +1 more source

Vector Biology Boot Camp Toolkit [PDF]

open access: yes
The Vector Biology Boot Camp is a program offered by the Northeast Regional Center for Excellence in Vector-Borne Diseases to provide hands-on learning opportunities in vector surveillance and control program operations.
Northeast Regional Center for Excellence in Vector-Borne Diseases
core   +4 more sources

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