Ask about this productRelated genes to: PENK antibody
- Gene:
- PDYN NIH gene
- Name:
- prodynorphin
- Previous symbol:
- SCA23
- Synonyms:
- PENKB, ADCA
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
- Gene:
- PENK NIH gene
- Name:
- proenkephalin
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-11-01
Related products to: PENK antibody
Related articles to: PENK antibody
- Prenatal opioid exposure (POE) can disrupt the development of dopamine and opioid systems, potentially altering behavioral sensitization in adulthood. - Source: PubMed
Publication date: 2026/04/10
Aaron Chantal C AVassoler Fair MByrnes Elizabeth M - Opioid addiction is a major public health problem that causes impairments in cognitive and oxidative processes. The present study has been designed to investigate the therapeutic potential of aerobic exercise, combined with herbal supplements (Rosa Canina L, Matricaria recutita, and Berberis), on oxidative stress and spatial learning during morphine withdrawal. - Source: PubMed
Publication date: 2025/08/26
Zibandeh Pour MahboubehTaghian FarzanehJalali Dehkordi Khosro - The increasing age of surgical patients is associated with a higher prevalence of chronic pain and cardiovascular comorbidities, including heart failure (HF). Recent studies suggest the existence of an intrinsic cardiac opioid system that may be dynamically regulated during HF. This study investigated left ventricular myocardial tissue from patients with end-stage dilated (DCM) and/or hypertrophic obstructive cardiomyopathy (HOCM) to assess whether the expression of opioid receptors and their endogenous ligand precursor peptides varies with cardiomyopathy type and severity. It was hypothesized that the cardiac opioid system is differentially regulated in DCM and HOCM, reflecting disease-specific remodeling. - Source: PubMed
Publication date: 2025/09/10
Lasch AlexandraShahin KholodShaqura MohammedDehé LukasCelik Melih ÖMousa Shaaban AHeidecker BettinaKnosalla ChristophSchäfer MichaelTreskatsch Sascha - It has been shown previously that repeated positive fighting experience in daily agonistic interactions is accompanied by the development of psychosis-like behavior, with signs of an addiction-like state associated with changes in the expression of genes encoding the proteins involved in the main neurotransmitter events in some brain regions of aggressive male mice. Fighting deprivation (a no-fight period of 2 weeks) causes a significant increase in their aggressiveness. This paper is aimed at studying-after a period of fighting deprivation-the involvement of genes (associated with neurotransmitter systems within the nucleus accumbens) in the above phenomena. The nucleus accumbens is known to participate in reward-related mechanisms of aggression. We found the following differentially expressed genes (DEGs), whose expression significantly differed from that in controls and/or mice with positive fighting experience in daily agonistic interactions followed by fighting deprivation: catecholaminergic genes , , , , , and ; serotonergic genes , , , and ; opioidergic genes , , and ; and glutamatergic genes , , , , , , , and . The expression of DEGs encoding proteins of the GABAergic system in experienced aggressive male mice mostly returned to control levels after fighting deprivation, except for . In light of the conceptual paradigm for analyzing data that was chosen in our study, the aforementioned DEGs associated with the behavioral pathology can be considered responsible for consequences of aggression followed by fighting deprivation, including mechanisms of an aggression relapse. - Source: PubMed
Publication date: 2025/09/03
Kudryavtseva Natalia NSmagin Dmitry ARedina Olga EKovalenko Irina LGalyamina Anna GBabenko Vladimir N
- Source: PubMed