Редактирование: ALDH1A1

Retinal dehydrogenase 1 (EC 1.2.1.-) (EC 1.2.1.36) (RALDH 1) (RalDH1) (ALDH-E1) (ALHDII) (Aldehyde dehydrogenase family 1 member A1) (Aldehyde dehydrogenase, cytosolic) [ALDC] [ALDH1] [PUMB1]

==Publications==

{{medline-entry
|title=Contribution of senescence in human endometrial stromal cells during proliferative phase to embryo receptivity†.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32285109
|abstract=Successful assisted reproductive technology pregnancy depends on the viability of embryos and endometrial receptivity. However, the literature has neglected effects of the endometrial environment during the proliferative phase on implantation success or failure. Human endometrial stromal cells (hESCs) were isolated from endometrial tissues sampled at oocyte retrieval during the proliferative phase from women undergoing infertility treatment. Primary hESC cultures were used to investigate the relationship between stemness and senescence induction in this population and embryo receptivity. Patients were classified as receptive or non-receptive based on their pregnancy diagnosis after embryo transfer. Biomarkers of cellular senescence and somatic stem cells were compared between each sample. hESCs from non-receptive patients exhibited significantly higher (P < 0.01) proportions of senescent cells, mRNA expressions of [[[[CDKN2A]]]] and [[CDKN1A]] transcripts (P < 0.01), and expressions of genes encoding the senescence-associated secretory phenotype (P < 0.05). hESCs from receptive patients had significantly higher (P < 0.01) mRNA expressions of [[ABCG2]] and [[ALDH1A1]] transcripts. Our findings suggest that stemness is inversely associated with senescence induction in hESCs and, by extension, that implantation failure in infertility treatment may be attributable to a combination of senescence promotion and disruption of this maintenance function in this population during the proliferative phase of the menstrual cycle. This is a promising step towards potentially improving the embryo receptivity of endometrium. The specific mechanism by which implantation failure is prefigured by a loss of stemness among endometrial stem cells, and cellular senescence induction among hESCs, should be elucidated in detail in the future.

|keywords=* cellular senescence
* embryo receptivity
* endometrial stem cell
* human endometrial stromal cell
* infertility
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7313258
}}
{{medline-entry
|title=Aldehyde Dehydrogenase 1 making molecular inroads into the differential vulnerability of nigrostriatal dopaminergic neuron subtypes in Parkinson's disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25705376
|abstract=A preferential dysfunction/loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) accounts for the main motor symptoms of Parkinson's disease (PD), the most common degenerative movement disorder. However, the neuronal loss is not stochastic, but rather displays regionally selectivity, indicating the existence of different DA subpopulations in the SNpc. To identify the underlying molecular determinants is thereby instrumental in understanding the pathophysiological mechanisms of PD-related neuron dysfunction/loss and offering new therapeutic targets. Recently, we have demonstrated that aldehyde dehydrogenase 1 ([[ALDH1A1]]) is one such molecular determinant that defines and protects an SNpc DA neuron subpopulation preferentially affected in PD. In this review, we provide further analysis and discussion on the roles of [[ALDH1A1]] in the function and survival of SNpc DA neurons in both rodent and human brains. We also explore the feasibility of [[ALDH1A1]] as a potential biomarker and therapeutic target for PD. 

|keywords=* Aging
* Aldehyde dehydrogenase 1
* Dopaminergic neuron
* Neurodegeneration
* Parkinson’s disease
* Substantia nigra pars compacta
* α-synuclein
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4334846
}}
{{medline-entry
|title=Assessment of the risk of blastomere biopsy during preimplantation genetic diagnosis in a mouse model: reducing female ovary function with an increase in age by proteomics method.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24156634
|abstract=Preimplantation genetic diagnosis ([[PGD]]) is important for screening genetic and chromosome mutations in embryos so that the efficiency of assisted reproductive treatment can be increased and birth defects can be decreased; however, some studies have reported a risk from this technology as well as other assisted reproductive technologies. We have developed a blastomere biopsy mouse model to assess the potential effects of blastomere biopsy that was one key procedure in [[PGD]] on the fertility of female mice at different ages. We showed that female fertility was decreased in the biopsied mouse model with an increase in age. Moreover, the ovarian weight, serum hormone levels, and the number of primordial, primary, preantral, and antral stage follicles were also decreased in the middle-aged biopsied mouse model. To elucidate the underlying molecular mechanism, we did proteomics analysis on ovarian tissues from puberty biopsied and nonbiopsied mice of the 23 differentially expressed proteins that were screened for in both groups, 3 proteins ([[PSMB8]], [[ALDH1A1]], and [[HSPA4]]) were selected and identified by Western blotting and quantitative RT-PCR methods, which showed the 3 proteins to regulate 12 cellular pathways. Furthermore, these three proteins were shown to be located in ovarian tissues, and the dynamic changes of expression profiling in middle-aged biopsied and nonbiopsied mice were demonstrated. The present study showed that blastomere biopsy technology impairs fertility when mice are middle-aged, which possibly resulted in abnormal expression profiling of [[PSMB8]], [[ALDH1A1]], and [[HSPA4]] proteins. Thus, additional studies should be performed to assess the overall risk of blastomere biopsies during [[PGD]] procedures. 
|mesh-terms=* Aging
* Aldehyde Dehydrogenase
* Aldehyde Dehydrogenase 1 Family
* Animals
* Biopsy
* Blastomeres
* Female
* Fertility
* Gene Expression Profiling
* Gene Expression Regulation
* Genes, Regulator
* HSP110 Heat-Shock Proteins
* Humans
* Mice
* Ovary
* Pregnancy
* Preimplantation Diagnosis
* Proteasome Endopeptidase Complex
* Retinal Dehydrogenase
* Signal Transduction

|full-text-url=https://sci-hub.do/10.1021/pr400366j
}}
{{medline-entry
|title=Multiple and additive functions of [[ALDH3A1]] and [[ALDH1A1]]: cataract phenotype and ocular oxidative damage in Aldh3a1(-/-)/Aldh1a1(-/-) knock-out mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17567582
|abstract=[[ALDH3A1]] (aldehyde dehydrogenase 3A1) is abundant in the mouse cornea but undetectable in the lens, and [[ALDH1A1]] is present at lower (catalytic) levels in the cornea and lens. To test the hypothesis that [[ALDH3A1]] and [[ALDH1A1]] protect the anterior segment of the eye against environmentally induced oxidative damage, Aldh1a1(-/-)/Aldh3a1(-/-) double knock-out and Aldh1a1(-/-) and Aldh3a1(-/-) single knock-out mice were evaluated for biochemical changes and cataract formation (lens opacification). The Aldh1a1/Aldh3a1- and Aldh3a1-null mice develop cataracts in the anterior and posterior subcapsular regions as well as punctate opacities in the cortex by 1 month of age. The Aldh1a1-null mice also develop cataracts later in life (6-9 months of age). One- to three-month-old Aldh-null mice exposed to UVB exhibited accelerated anterior lens subcapsular opacification, which was more pronounced in Aldh3a1(-/-) and Aldh3a1(-/-)/Aldh1a1(-/-) mice compared with Aldh1a1(-/-) and wild type animals. Cataract formation was associated with decreased proteasomal activity, increased protein oxidation, increased GSH levels, and increased levels of 4-hydroxy-2-nonenal- and malondialdehyde-protein adducts. In conclusion, these findings support the hypothesis that corneal [[ALDH3A1]] and lens [[ALDH1A1]] protect the eye against cataract formation via nonenzymatic (light filtering) and enzymatic (detoxification) functions.
|mesh-terms=* Aging
* Aldehyde Dehydrogenase
* Aldehyde Dehydrogenase 1 Family
* Animals
* Cataract
* Cornea
* Eye Proteins
* Glutathione
* Lens, Crystalline
* Mice
* Mice, Knockout
* Oxidation-Reduction
* Oxidative Stress
* Phenotype
* Proteasome Endopeptidase Complex
* Retinal Dehydrogenase
* Ultraviolet Rays

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2253645
}}