User Guide
Why can I only view 3 results?
You can also view all results when you are connected from the network of member institutions only. For non-member institutions, we are opening a 1-month free trial version if institution officials apply.
So many results that aren't mine?
References in many bibliographies are sometimes referred to as "Surname, I", so the citations of academics whose Surname and initials are the same may occasionally interfere. This problem is often the case with citation indexes all over the world.
How can I see only citations to my article?
After searching the name of your article, you can see the references to the article you selected as soon as you click on the details section.
 ASOS INDEKS
 Views 8
Transmembrane 29 (Tmem29), a Newly Identified Molecule Showed Downregulation in Hypoxic-Ischemic Brain Damage
2022
Journal:  
NeuroSci
Author:  
Abstract:

: Transmembrane 29 ( Tmem29) gene with unknown function is a gene located on the X chromosome of the mouse genome. The gene showed differential expression in the Vannucci neonatal hypoxic-ischemic mouse brain model. We found the gene expresses with different molecular forms, including a group of long non-coding RNA forming a family of transcripts. It was predominantly expressed in the testes, brain, and kidney of mouse. In vitro identification and functional characterization were carried out in Neuro2a cells. Using fluorescence microscopy, Tmem29 protein was found to be constitutively expressed in mouse cell lines of different origins. Oxygen glucose deprivation (OGD) induced apoptotic cell death in Neuro2a cells and was confirmed by activations of caspase 3. Tmem29 protein was found to be associated with cell death especially at the time points of caspase 3 activations. A similar response was obtained in glucose deprivation (GD) cultures suggesting Tmem29 response to a common mechanism induced by OGD and GD. Downregulation of Tmem29 was induced by OGD and GD, further validating its response to hypoxia-ischemia (HI) insults. Our findings contributed to further understanding of molecular events after hypoxic-ischemic insults and opens new avenues for developing protective and therapeutic strategies for hypoxic-ischemic encephalopathy or even pathological programmed cell death.

Keywords:

null
2022
Journal:  
NeuroSci
Author:  
0
2022
Journal:  
NeuroSci
Author:  
Keywords:

Citation Owners
Information: There is no ciation to this publication.
Similar Articles












NeuroSci

Journal Type :   Uluslararası

NeuroSci