Regulation of the human ether-a-go-go-related gene (hERG) potassium channel by Nedd4 family interacting proteins (Ndfips)

2015 ◽  
Vol 472 (1) ◽  
pp. 71-82 ◽  
Author(s):  
Yudi Kang ◽  
Jun Guo ◽  
Tonghua Yang ◽  
Wentao Li ◽  
Shetuan Zhang
Keyword(s):  
Potassium Channel ◽  
Precursor Cell ◽  
K Channel ◽  
Neural Precursor ◽  
Cardiac Repolarization ◽  
Interacting Proteins ◽  
Neural Precursor Cell ◽  
Related Gene ◽  
Cellular Compartments ◽  
Herg Channels

The human ether-a-go-go-related gene (hERG)-encoded K+ channel is critical for cardiac repolarization. In the present study, we demonstrate that the E3 ubiquitin (Ub) ligase neural precursor cell expressed developmentally down-regulated protein 4-2 (Nedd4-2) is directed to specific cellular compartments by Nedd4 family-interacting proteins (Ndfips) to selectively target the mature hERG channels for degradation.

How to Fluorescently Label the Potassium Channel: A Case in hERG

2020 ◽  
Vol 27 (18) ◽  
pp. 3046-3054
Author(s):  
Xiaomeng Zhang ◽  
Beilei Wang ◽  
Zhenzhen Liu ◽  
Yubin Zhou ◽  
Lupei Du
Keyword(s):  
Potassium Channel ◽  
Herg Channel ◽  
Pore Channel ◽  
Design Rationale ◽  
Related Gene ◽  
Open Conformation ◽  
Cardiac Action ◽  
Qt Syndrome ◽  
Herg Channels ◽  
Action Potential Repolarization

hERG (Human ether-a-go-go-related gene) potassium channel, which plays an essential role in cardiac action potential repolarization, is responsible for inherited and druginduced long QT syndrome. Recently, the Cryo-EM structure capturing the open conformation of hERG channel was determined, thus pushing the study on hERG channel at 3.8 Å resolution. This report focuses primarily on summarizing the design rationale and application of several fluorescent probes that target hERG channels, which enables dynamic and real-time monitoring of potassium pore channel affinity to further advance the understanding of the channels.

A Review of Bioreactor Protocols for Human Neural Precursor Cell Expansion in Preparation for Clinical Trials

2011 ◽  
Vol 6 (3) ◽  
pp. 229-254 ◽  
Author(s):  
Behnam A. Baghbaderani ◽  
Karim Mukhida ◽  
Murray Hong ◽  
Ivar Mendez ◽  
Leo A. Behie
Keyword(s):  
Clinical Trials ◽  
Cell Expansion ◽  
Precursor Cell ◽  
Neural Precursor ◽  
Neural Precursor Cell

Sonic Hedgehog Regulation of the Neural Precursor Cell Fate During Chicken Optic Tectum Development

2017 ◽  
Vol 64 (2) ◽  
pp. 287-299 ◽  
Author(s):  
Ciqing Yang ◽  
Xiaoying Li ◽  
Qiuling Li ◽  
Han Li ◽  
Liang Qiao ◽  
...  
Keyword(s):  
Cell Fate ◽  
Sonic Hedgehog ◽  
Optic Tectum ◽  
Precursor Cell ◽  
Neural Precursor ◽  
Neural Precursor Cell

Neural precursor cell influences on blood–brain barrier characteristics in rat brain endothelial cells

2007 ◽  
Vol 1159 ◽  
pp. 67-76 ◽  
Author(s):  
Joseph C. Lim ◽  
Adam J. Wolpaw ◽  
Maeve A. Caldwell ◽  
Stephen B. Hladky ◽  
Margery A. Barrand
Keyword(s):  
Endothelial Cells ◽  
Rat Brain ◽  
Blood Brain Barrier ◽  
Precursor Cell ◽  
Brain Barrier ◽  
Neural Precursor ◽  
Brain Endothelial Cells ◽  
Neural Precursor Cell ◽  
Blood Brain ◽  
Rat Brain Endothelial Cells

Bioengineering Protocols for Neural Precursor Cell Expansion

2009 ◽  
pp. 105-123 ◽  
Author(s):  
Behnam A. Baghbaderani ◽  
Arindom Sen ◽  
Michael S. Kallos ◽  
Leo A. Behie
Keyword(s):  
Cell Expansion ◽  
Precursor Cell ◽  
Neural Precursor ◽  
Neural Precursor Cell

scholarly journals The Role of Mcl-1 in Embryonic Neural Precursor Cell Apoptosis

2021 ◽  
Vol 9 ◽  
Author(s):  
Robert T. Flemmer ◽  
Sarah P. Connolly ◽  
Brittany A. Geizer ◽  
Joseph T. Opferman ◽  
Jacqueline L. Vanderluit
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Precursor Cell ◽  
Embryonic Lethality ◽  
Conditional Knockout ◽  
Neural Precursor ◽  
Null Mouse ◽  
Neural Precursor Cell ◽  
Thoracic Spinal Cord

Myeloid cell leukemia-1 (Mcl-1), an anti-apoptotic Bcl-2 protein, regulates neural precursor cell (NPC) survival in both the developing and adult mammalian nervous system. It is unclear when during the neurogenic period Mcl-1 becomes necessary for NPC survival and whether Bax is the sole pro-apoptotic target of Mcl-1. To address these questions, we used the nervous system-specific Nestin-Cre Mcl-1 conditional knockout mouse line (Mcl-1 CKO) to assess the anti-apoptotic role of Mcl-1 in developmental neurogenesis. Loss of Mcl-1 resulted in a wave of apoptosis beginning in the brainstem and cervical spinal cord at embryonic day 9.5 (E9.5) and in the forebrain at E10.5. Apoptosis was first observed ventrally in each region and spread dorsally over time. Within the spinal cord, apoptosis also spread in a rostral to caudal direction following the path of differentiation. Breeding the Mcl-1 CKO mouse with the Bax null mouse rescued the majority of NPC from apoptosis except in the dorsomedial brainstem and ventral thoracic spinal cord where only 50% were rescued. This demonstrates that Mcl-1 promotes NPC survival primarily by inhibiting the activation of Bax, but that Bax is not the sole pro-apoptotic target of Mcl-1 during embryonic neurogenesis. Interestingly, although co-deletion of Bax rescued the majority of NPC apoptosis, it resulted in embryonic lethality at E13, whereas conditional deletion of both Mcl-1 and Bax rescued embryonic lethality. In summary, this study demonstrates the widespread dependency on Mcl-1 during nervous system development.

DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3

Development ◽  
2001 ◽  
Vol 128 (1) ◽  
pp. 137-146
Author(s):  
C. D'Sa-Eipper ◽  
J.R. Leonard ◽  
G. Putcha ◽  
T.S. Zheng ◽  
R.A. Flavell ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cell Apoptosis ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Precursor Cell ◽  
Neural Precursor ◽  
Normal Brain ◽  
Neural Precursor Cell ◽  
Caspase 9

Programmed cell death (apoptosis) is critical for normal brain morphogenesis and may be triggered by neurotrophic factor deprivation or irreparable DNA damage. Members of the Bcl2 and caspase families regulate neuronal responsiveness to trophic factor withdrawal; however, their involvement in DNA damage-induced neuronal apoptosis is less clear. To define the molecular pathway regulating DNA damage-induced neural precursor cell apoptosis, we have examined the effects of drug and gamma-irradiation-induced DNA damage on telencephalic neural precursor cells derived from wild-type embryos and mice with targeted disruptions of apoptosis-associated genes. We found that DNA damage-induced neural precursor cell apoptosis, both in vitro and in vivo, was critically dependent on p53 and caspase 9, but neither Bax nor caspase 3 expression. Neural precursor cell apoptosis was also unaffected by targeted disruptions of Bclx and Bcl2, and unlike neurotrophic factor-deprivation-induced neuronal apoptosis, was not associated with a detectable loss of cytochrome c from mitochondria. The apoptotic pathway regulating DNA damage-induced neural precursor cell death is different from that required for normal brain morphogenesis, which involves both caspase 9 and caspase 3 but not p53, indicating that additional apoptotic stimuli regulate neural precursor cell numbers during telencephalic development.

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