Ask about this productRelated genes to: RGS12 antibody
- Gene:
- RGS12 NIH gene
- Name:
- regulator of G protein signaling 12
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-24
- Date modifiied:
- 2017-04-13
Related products to: RGS12 antibody
Related articles to: RGS12 antibody
- Acute myocardial infarction (AMI) is one of the leading causes of death worldwide. Timely reperfusion therapy following AMI can effectively salvage ischemic cardiomyocytes. However, myocardial ischemia-reperfusion injury (MIRI), which inevitably occurs during the process of blood supply recovery, may affect the therapeutic outcome. During MIRI, various forms of cell death, such as apoptosis, autophagy and pyroptosis, are involved. Ferroptosis is a recently discovered form of programmed cell death. Studies have shown that ferroptosis is closely related to the progression of MIRI. In the regulation of ferroptosis, GPX4 inhibits ferroptosis by clearing lipid peroxides, whereas ACSL4 promotes lipid peroxidation and drives ferroptosis. In addition to known regulatory factors, recent studies have found that Regulator of RGS12, a key protein in the RGS family, plays an important role in ischemia-reperfusion injury. The deletion of Regulator of RGS12 significantly reduces the incidence of ferroptosis in cardiomyocytes, whereas its overexpression exacerbates ferroptosis. This phenomenon may be related to the regulation of iron metabolism-related signaling pathways by RGS12. This review aims to summarize the molecular mechanisms by which RGS12 influences the progression of ferroptosis through regulating GPX4 and ACSL4 expression, thereby contributing to MIRI. - Source: PubMed
Publication date: 2026/03/27
Zi CongnaZhang ZhiweiZhang Tao - Depression in older adults has been associated with negative health outcomes, such as dementia. Previous research has demonstrated that green and blue spaces, defined as areas of vegetation or bodies of water respectively, are beneficial to mental health, although the biological mechanisms are poorly understood. One of the mechanisms proposed is DNA methylation (DNAm). DNAm is an epigenetic process that alters gene expression. Changes in methylation have been observed in those with depression, and associated with green space exposure, while blue spaces have been shown to reduce the risk of depression. Using a mechanistic review approach, we investigated the relationships of green space and depression with DNAm with the aim of identifying potential overlapping mechanisms. In the environmental search, keywords such as 'green space' and 'DNAm' were combined. In the mental health search, keywords such as 'DNAm' and 'depression' were combined. From a total of 45 695 papers returned, four studies on green space, and five studies on depression met the eligibility criteria for this review. All included studies reported significant or suggestively significant methylation sites. No overlapping CpG sites were identified when comparing methylation changes found in response to green space and depression. Changes in the gene were associated with both depression and green space exposure. DNAm is a biological mechanism that may contribute to the impact of exposure to green space; further research is warranted to better understand DNAm as a mechanistic pathway between green space and depression. - Source: PubMed
Publication date: 2026/03/14
Illyuk JacobGlover SophieWalsh Shea AJurek-Loughrey AnnaMcKnight Amy JayneHunter Ruth F - Mitochondrial function and its regulation within the placenta are critical for maintaining a healthy pregnancy. This study investigated the role of G-protein signaling 12 (RGS12) in placental mitochondrial function and pregnancy outcomes. RGS12 was found to be localized within the mitochondria of placental trophoblast cells. RGS12 knockdown in human placental cells resulted in decreased mitochondrial abundance, impaired oxidative phosphorylation, and reduced antioxidant capacity. Mechanistically, RGS12 enhanced the function of ATP5B, a key mitochondrial enzyme, by promoting its tyrosine phosphorylation. In a mouse model, placental RGS12 deficiency led to reduced tolerance to preterm birth (PTB) challenge, decreased fetal weight, and trophoblast cell death. These adverse effects were associated with diminished ATP synthase activity and activation of the p38MAPK signaling pathway, while restoring RGS12 expression improved the phenotype of mitochondrial dysfunction in placental trophoblast cells. Furthermore, reduced RGS12 expression and impaired mitochondrial function were observed in placentas from cases experiencing PTB. Collectively, these findings provide hitherto undocumented evidence of a specific molecular mechanism by which placental mitochondrial dysfunction contributes to adverse pregnancy outcomes. Our study suggests that RGS12 may represent a novel therapeutic target for improving pregnancy outcomes through its role in regulating placental mitochondrial function. - Source: PubMed
Publication date: 2026/02/09
Cao XianlingZhou XuanyouXu NaixinShi WeihuiHuang HefengSun ZhengaoChen SongchangXu Chen-Ming - Sexual maturation in boars impacts reproductive efficiency in swine production, yet the molecular mechanisms underlying this developmental transition remain poorly understood. This study aimed to investigate the transcriptomic changes in sperm from Duroc boars during sexual maturation, conducting a longitudinal analysis. The total RNA and miRNA profiles from the same individuals (n = 6) at puberty (7.24 ± 0.39 months) and sexual maturity (10 ± 0.40 months) were compared, identifying molecular signatures associated with reproductive development. Total RNA sequencing (Illumina NovaSeq-6000) and miRNA sequencing (Illumina NextSeq-500) were performed on all 12 paired samples (6 boars at 2 time points), followed by differential expression analysis using a paired statistical model in DESeq2 to account for repeated measures. - Source: PubMed
Publication date: 2026/01/21
Shrestha Asmitavan Son MarenHashim AdnanRouzbehani SoudabehGilfillan Gregor DBerge UrszulaKommisrud ElisabethAlm-Kristiansen Anne Hege - Our goal in this study was to determine whether functional variation in the human gene influences behavioral responses to psychostimulants such as methylphenidate, thereby informing whether such genetic findings should affect the clinical use of this central nervous system (CNS)-stimulating agent in bipolar disorder (BD) patients with comorbid attention-deficit/hyperactivity disorder (ADHD). The use of psychostimulants for ADHD in BD remains controversial due to concerns about mood destabilization, although recent systematic reviews indicate that methylphenidates and amphetamines can be safe and effective when used with mood stabilizers. RGS12, a striatally enriched regulator of κ-opioid receptor signaling and dopamine transporter (DAT) function, has been implicated in altered dopaminergic responses to psychostimulants. A recently characterized R59Q reduction-of-function mutation within RGS12 has been associated with familial bipolar disorder, further highlighting its potential relevance to mood and psychostimulant responsiveness. -deficient mice were evaluated for behavioral responses to methylphenidate (i.e., locomotor hyperactivity) and compared with responses to dopamine transporter-dependent stimulants. deficiency was seen to reduce hyperlocomotion with amphetamine, and with methamphetamine but not with methylphenidate, which was instead observed to elicit normal hyperlocomotor responses across all doses. Methylphenidate responsiveness remains intact despite the loss of RGS12 function, suggesting that functional variation in the human condition should not contraindicate methylphenidate use in mood-stabilized BD/ADHD comorbidity. - Source: PubMed
Publication date: 2025/12/12
Agogo-Mawuli Percy SGross Joshua DSetola VincentGall Bryan JSiderovski David P