Редактирование: NLRX1

NLR family member X1 precursor (Caterpiller protein 11.3) (CLR11.3) (Nucleotide-binding oligomerization domain protein 26) (Nucleotide-binding oligomerization domain protein 5) (Nucleotide-binding oligomerization domain protein 9) [NOD26] [NOD5] [NOD9]

==Publications==

{{medline-entry
|title=NOD-like receptor X1 functions as a tumor suppressor by inhibiting epithelial-mesenchymal transition and inducing aging in hepatocellular carcinoma cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29482578
|abstract=This study was performed to investigate the role of nucleotide-binding oligomerization domain (NOD)-like receptor X1 ([[NLRX1]]) in regulating hepatocellular carcinoma (HCC) progression. Expression levels of [[NLRX1]] in clinical specimens and cell lines were determined by reverse transcription-polymerase chain reaction (RT-PCR) and western blot (WB). Transwell assays were conducted to evaluate the effect of [[NLRX1]] on cell invasion, and flow cytometry was used to assess apoptosis. Expression patterns of key molecules in the phosphoinositide 3-kinase (PI3K)-AKT pathways were determined via WB. The effect of [[NLRX1]] on cell senescence was evaluated with β-galactosidase assays. Kaplan-Meier analyses and Cox regression models were used for prognostic evaluation. [[NLRX1]] was downregulated in tumor tissue compared with adjacent normal liver tissue. Low tumor [[NLRX1]] expression was identified as an independent indicator for HCC prognosis (recurrence: hazard ratio [HR] 1.87, 95% confidence interval [CI] 1.26-2.76, overall survival [OS] 2.26, 95% CI 1.44-3.56). [[NLRX1]] over-expression (OE) significantly inhibited invasiveness ability and induced apoptosis in HCC cells. In vivo experiments showed that [[NLRX1]] knock-down (KD) significantly promoted HCC growth. Mechanistically, [[NLRX1]] exhibited a suppressor function by decreasing phosphorylation of AKT and thus downregulating Snail1 expression, which inhibited epithelial-mesenchymal-transition (EMT) in HCC cells. Moreover, [[NLRX1]] OE could induce cell senescence via an AKT-P21-dependent manner. [[NLRX1]] acted as a tumor suppressor in HCC by inducing apoptosis, promoting senescence, and decreasing invasiveness by repressing PI3K-AKT signaling pathway. Future investigations will focus on restoring expression of [[NLRX1]] to provide new insights into HCC treatment.
|mesh-terms=* Animals
* Carcinoma, Hepatocellular
* Cell Line, Tumor
* Cellular Senescence
* Epithelial-Mesenchymal Transition
* Female
* Gene Expression Regulation, Neoplastic
* Humans
* Liver Neoplasms
* Male
* Mice, Nude
* Middle Aged
* Mitochondrial Proteins
* Phosphatidylinositol 3-Kinases
* Prognosis
* Proto-Oncogene Proteins c-akt
* Signal Transduction
|keywords=* Epithelial-mesenchymal-transition
* Hepatocellular carcinoma
* NLRX1
* Senescence
* Transition
* Tumor suppressor
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5828065
}}
{{medline-entry
|title=The expression of [[NLRX1]] in C57BL/6 mice cochlear hair cells: Possible relation to aging- and neomycin-induced deafness.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26836140
|abstract=Nucleotide-binding domain and leucine-rich-repeat-containing family member X1 ([[NLRX1]]) is a cytoplasmic pattern recognition receptor that is predominantly located in mitochondria, which is tightly related to mitochondrial damage, reactive oxygen species (ROS) production, inflammation and apoptosis. The present study was designed to explore whether [[NLRX1]] expresses in C57BL/6 mice cochlear hair cells and, if so, to investigate the possible correlations between [[NLRX1]] and hearing. The location and dynamic expression of [[NLRX1]] were investigated by immunofluorescence, real-time PCR and Western blotting. Hearing thresholds of C57BL/6 mice were measured by auditory brainstem response (ABR). Moreover, the downstream inflammatory and apoptotic pathways regulated by [[NLRX1]] were examined in age-related and neomycin-induced hair cell damage. Data showed that [[NLRX1]] expressed in cytoplasm of C57BL/6 cochlear hair cells, especially in the cilia, which were essential for sound sensation. The expression of [[NLRX1]] in hair cells increased as the mice grew up, and, decreased as they aged. Additionally, the activated apoptotic JNK pathway was detected in 9-month old mice with worse-hearing and 3-month old mice treated with neomycin. Overall, results indicate that [[NLRX1]] may relate to hair cell maturity, hearing formation and maintenance, and promote hair cell apoptosis through JNK pathway induced by aging and neomycin.
|mesh-terms=* Aging
* Animals
* Animals, Newborn
* Anti-Bacterial Agents
* Apoptosis
* Deafness
* Evoked Potentials, Auditory, Brain Stem
* Hair Cells, Auditory
* Mice, Inbred C57BL
* Mitochondrial Proteins
* Neomycin
|keywords=* Apoptosis
* C57BL/6 mice
* Hair cells
* NLRX1
* Nucleotide-binding domain and leucine-rich-repeat-containing family member X1
|full-text-url=https://sci-hub.do/10.1016/j.neulet.2015.11.053
}}