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
- 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 - Sex differences in pain sensitivity and response to analgesics are well-documented, with females often experiencing higher pain sensitivity and different responses to pain treatments compared to males. While Regulator of G-protein Signaling 12 (RGS12) is crucial in the central nervous system, its role in the peripheral nervous system and pain modulation remains unclear. Putative nociceptor-specific RGS12 conditional knockout (Rgs12-cKO) mice were generated by crossing Rgs12 floxed (Ctrl) mice with Trpv1-Cre transgenic mice. Behavioral assays, including the von Frey microfilament, hot plate, running wheel, and conditioned place preference, were conducted to assess pain sensitivity. Dorsal root ganglion (DRG) neurons from both sexes were dissected and cultured to examine neurite outgrowth and relative Ca²⁺ fluorescence (ΔF/F₀). Immunofluorescence, Ca imaging, quantitative real-time PCR, and Western blot analyses were performed to investigate molecular and cellular mechanisms. Female Rgs12-cKO mice exhibited decreased pain sensitivity to both mechanical and thermal stimuli and reduced neurite outgrowth in DRG neurons. In contrast, male Rgs12-cKO mice did not show significant differences compared to Ctrl mice. The expression of estrogen receptors, particularly Gper, dramatically increased in Rgs12-cKO females but not males. GPER-specific agonist G1 and GPER-specific inhibitor CIMBA stimulation differentially increased KCl-induced relative Ca²⁺ fluorescence in DRG neurons from male and female mice, highlighting a sex-dependent response. This study demonstrates that RGS12 plays a critical role in modulating pain sensitivity in a sex-dependent manner. The interplay between RGS12 and estrogen/GPER signaling pathways in DRG neurons underscores the importance of RGS12 in considering sex as a critical biological variable in pain research. PERSPECTIVE: This study reveals RGS12 as a key regulator of sex-dependent pain modulation through estrogen/GPER-mediated calcium signaling in sensory neurons. The findings provide mechanistic insight into sex differences in nociception and suggest RGS12 as a potential therapeutic target for female-predominant pain disorders. - Source: PubMed
Publication date: 2025/12/04
Rao ChunbaoGautam MayankYang Shu-TingLuo WenqinYang Shuying