Results 11 to 20 of about 1,734,521 (378)

Nonlinear Protein Degradation and the Function of Genetic Circuits [PDF]

open access: yes, 2005
The functions of most genetic circuits require sufficient degrees of cooperativity in the circuit components. While mechanisms of cooperativity have been studied most extensively in the context of transcriptional initiation control, cooperativity from other processes involved in the operation of the circuits can also play important roles. In this study,
Ali Azam   +43 more
arxiv   +4 more sources

Identification of a WNT5A-Responsive Degradation Domain in the Kinesin Superfamily Protein KIF26B. [PDF]

open access: yes, 2018
Noncanonical WNT pathways function independently of the β-catenin transcriptional co-activator to regulate diverse morphogenetic and pathogenic processes.
Choi, Shannon S   +6 more
core   +2 more sources

Gambogic Acid Is a Tissue-Specific Proteasome Inhibitor In Vitro and In Vivo

open access: yesCell Reports, 2013
Gambogic acid (GA) is a natural compound derived from Chinese herbs that has been approved by the Chinese Food and Drug Administration for clinical trials in cancer patients; however, its molecular targets have not been thoroughly studied.
Xiaofen Li   +28 more
doaj   +1 more source

Hyperglycemia triggers HIPK2 protein degradation [PDF]

open access: yes, 2016
Homeodomain interacting protein kinase-2 (HIPK2) is an evolutionary conserved kinase that modulates several key molecular pathways to restrain tumor growth and induce p53-depending apoptotic cell-death in response to anticancer therapies. HIPK2 silencing
Baldari, Silvia   +6 more
core   +2 more sources

Nickel pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via both Bcr/Abl-dependent and Bcr/Abl-independent mechanisms

open access: yesJournal of Hematology & Oncology, 2016
Background Acquired imatinib (IM) resistance is frequently characterized by Bcr-Abl mutations that affect IM binding and kinase inhibition in patients with chronic myelogenous leukemia (CML).
Xiaoying Lan   +13 more
doaj   +1 more source

Regulation of CLC-1 chloride channel biosynthesis by FKBP8 and Hsp90β. [PDF]

open access: yes, 2016
Mutations in human CLC-1 chloride channel are associated with the skeletal muscle disorder myotonia congenita. The disease-causing mutant A531V manifests enhanced proteasomal degradation of CLC-1.
Chen, Shu-Ching   +7 more
core   +1 more source

UPRmt and coordinated UPRER in type 2 diabetes

open access: yesFrontiers in Cell and Developmental Biology, 2022
The mitochondrial unfolded protein response (UPRmt) is a molecular mechanism that maintains mitochondrial proteostasis under stress and is closely related to various metabolic diseases, such as type 2 diabetes (T2D).
Zhanfang Kang   +6 more
doaj   +1 more source

Friends in need: how chaperonins recognize and remodel proteins that require folding assistance [PDF]

open access: yesFront. Mol. Biosci. (2022) 9:1071168, 2022
Chaperonins are biological nanomachines that help newly translated proteins to fold by rescuing them from kinetically trapped misfolded states. Protein folding assistance by the chaperonin machinery is obligatory in vivo for a subset of proteins in the bacterial proteome.
arxiv   +1 more source

An eIF4E-binding protein regulates katanin protein levels in C. elegans embryos. [PDF]

open access: yes, 2009
In Caenorhabditis elegans, the MEI-1-katanin microtubule-severing complex is required for meiosis, but must be down-regulated during the transition to embryogenesis to prevent defects in mitosis.
DeBella, Leah   +4 more
core   +2 more sources

Erioflorin stabilizes the tumor suppressor Pdcd4 by inhibiting its interaction with the E3-ligase β-TrCP1 [PDF]

open access: yes, 2012
Loss of the tumor suppressor Pdcd4 was reported for various tumor entities and proposed as a prognostic marker in tumorigenesis. We previously characterized decreased Pdcd4 protein stability in response to mitogenic stimuli, which resulted from p70S6K1 ...
Bajer, Magdalena M.   +11 more
core   +6 more sources

Home - About - Disclaimer - Privacy