Ask about this productRelated genes to: FKBP5 Blocking Peptide
- Gene:
- FKBP4 NIH gene
- Name:
- FKBP prolyl isomerase 4
- Previous symbol:
- -
- Synonyms:
- FKBP59, FKBP52
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-14
- Date modifiied:
- 2018-11-01
- Gene:
- FKBP5 NIH gene
- Name:
- FKBP prolyl isomerase 5
- Previous symbol:
- -
- Synonyms:
- FKBP51, FKBP54, PPIase, P54, Ptg-10
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-09
- Date modifiied:
- 2018-11-01
Related products to: FKBP5 Blocking Peptide
Related articles to: FKBP5 Blocking Peptide
- Decidualization of human endometrial stromal cells (HESCs) is one of the critical steps in the establishment of human pregnancy. Nevertheless, little is known about the molecular mechanisms underlying human decidualization. In this study, we identified high-mobility group box transcription factor 1 (HBP1) as a key player in the decidualization of HESCs. Knockdown of HBP1 expression significantly reduced the mRNA and protein expression levels of the decidualization markers insulin-like growth factor-binding protein 1 (IGFBP1) and forkhead box O1 (FOXO1). Although progesterone receptor (PGR) expression did not significantly change, the expression levels of PGR-regulated target molecules decreased. Furthermore, ChIP-Seq and RNA-Seq analyses revealed that HBP1 directly transcriptionally regulates IGFBP1 expression. Additionally, overexpression of HBP1 promoted the enrichment of histone H3K4me3 at the promoter regions of PGR and its target molecules FK506 binding protein 5 (FKBP5), Fos-related antigen 2 (FRA-2/FOSL2), and FK506-binding protein 4 (FKBP4), which indicated that HBP1 enhances PGR transcriptional activity. Clinical specimen analysis further confirmed that the expression of HBP1 and PGR target molecules was significantly downregulated in the endometria of patients with recurrent implantation failure. In conclusion, this study provides evidence that HBP1 plays an important regulatory role in embryo implantation. - Source: PubMed
Publication date: 2026/01/18
Guo YuyingTian WencaiNie ChangjunHuang JiweiFan HuiliuChen ZhengqinLin ZhongQin AipingHuang Pinxiu - Adolescence is a sensitive window for the maturation of hypothalamic-pituitary-adrenal (HPA) axis function; however, the timing and mechanisms underlying this transition remain unclear, particularly in females and in response to repeated homotypic stress. We measured corticosterone (CORT) release and glucocorticoid-related gene expression in postpubertal (P45) and adult (P75) male and female rats after acute or repeated restraint. In males, adolescents elicited higher CORT responses than adults did after acute stress, although both ages showed habituation to repeated restraint. In contrast, females exhibited adult-like CORT responses by P45 and no evidence of habituation. At the molecular level, adolescents of both sexes displayed distinct medial prefrontal cortex and ventral hippocampus expression profiles of glucocorticoid receptor () and co-chaperones (, ) relative to adults, though these effects were more pronounced in females, for whom there were also age- and stress-dependent changes in mineralocorticoid receptor () expression. These findings suggest that while hormonal stress responses mature earlier in females than in males, sex-specific trajectories of molecular regulation continue to develop into late adolescence, potentially shaping long-term vulnerability to stress-related disorders. - Source: PubMed
Publication date: 2026/01/12
Burke Francine FLeonetti Amanda MLacasse Jesse MPirri FardadMcCormick Cheryl M - The biological consequences of chronic stress and trauma are complex, influencing multiple systems and contributing to the development of psychiatric disorders such as MDD and PTSD. Yet, the underlying molecular mechanisms that confer susceptibility in some individuals but resilience in others remain incompletely understood. To help close these knowledge gaps, my work centers on glucocorticoid signaling as a core mechanism underlying stress-related adaptations. This includes the glucocorticoid receptor (GR), its co-chaperones FKBP5 and FKBP4, and regulatory partners such as SKA2. Through a combination of genetic, viral, pharmacological, and transcriptomic approaches, my lab has delineated how these molecules influence HPA axis feedback, fear-related learning, and stress recovery. Recently, we identified a novel, GR-independent role for SKA2 in regulating secretory autophagy, a non-lytic autophagy pathway involved in vesicular cargo release, including cytokine secretion in microglia. These findings established a mechanistic link between intracellular stress signaling and neuroinflammatory responses. In a parallel line of research, we are investigating how chronic stress alters the gut microbiome composition and function, and how these changes impact behavior. Our aim is to harness dietary and probiotic interventions to restore homeostatic balance and enhance stress resilience. By integrating molecular neuroscience with immune and microbiome research, my long-term goal is to build a comprehensive, systems-level model of stress vulnerability and resilience. This approach holds promise for identifying novel biomarkers and therapeutic targets that support mental health and resilience across the lifespan. - Source: PubMed
Publication date: 2025/09/09
Hartmann Jakob - has been of special scientific interest in the behavioral sciences since it has been involved in the pathophysiology of several mental disorders. It is a gene with pleiotropic effects which encodes the protein FKBP5, a cochaperone that decreases glucocorticoid receptor (GR) affinity for glucocorticoids by competing with FKBP4, altering the GR chaperone complex, and impairing GR activation. As a key modulator of the stress response, FKBP5 plays a critical role in regulating cortisol levels in the organism. The gene is regulated through a combination of transcriptional, epigenetic, post-transcriptional, and environmental mechanisms, as well as genetic polymorphisms that influence its transcription and stress responsiveness. Notably, the rs1360780 T-allele in significantly affects FKBP5 regulation and has been linked to stress-related disorders by influencing transcription and stress responsiveness. In this narrative review, we aim to provide an overview of the role played by the single-nucleotide polymorphism rs1360780 in the locus in gene expression, its epigenetic regulation, and the impact of early stress in its functioning. We discuss some brain regions with differential expression of and some behavioral phenotypes linked to the locus. The T-allele of rs1360780 is considered a risk variant, as it leads to high induction, which delays negative feedback and increases GR resistance. This results in states of relative hypercortisolemia and brain morphofunctional alterations, particularly in regions sensitive to glucocorticoid activity during critical periods of neurodevelopment. Additionally, exposure to childhood maltreatment is associated with demethylation of the glucocorticoid response elements of , further increasing its expression levels. Among the psychological dimensions analyzed in which is involved are neurocognition, aggression, suicidality, and social cognition. At the level of mental disorders, the gene may play a role in the pathogenesis of post-traumatic stress disorder, depression, and bipolar disorder. In psychotic disorders, its role is less clear. This knowledge enhances the understanding of disease mechanisms that operate through psychopathological dimensions, and highlights the need to design specific, person-centered psychopharmacological and environmental therapeutic interventions. - Source: PubMed
Publication date: 2025/03/11
Arancibia MarceloManterola MarciaRíos UlisesMoya Pablo RMoran-Kneer JavierBustamante M Leonor - Glucocorticoids (GC) are the main treatment for pemphigus foliaceus (PF). The effects of GC are mediated through glucocorticoid receptors (GR), with GRα and GRβ being the most significant isoforms. Several molecules are involved in mediating the cellular response to GC and can affect the response to treatment. However, the relationship between sensitivity to GC and the expression of GRα, GRβ, FKBP5, FKBP4, HAT1 and HDAC2 in PF disease has not yet been studied. The purpose of this study was to determine the expression of these molecules in patients with different types of response to treatment. Quantitative real-time PCR was used for gene expression profiling in systemic and cutaneous levels. The protein expression levels of GRα and GRβ and FKBP5 was accomplished through immunohistochemical staining. We studied the association of rs1360780 > FKBP5 SNP with PF disease using TaqMan SNP genotyping. Our findings showed downregulation in the gene expression levels of GRα (p = 0.016), HDAC2 (p = 0.004) and FKBP5 (p = 0.032) genes in PF patients compared to healthy controls in PBMC and an up-regulation in GRα (p = 0.041) and HAT1 (p = 0.008) in remittent patients compared to newly diagnosed patients in skin biopsies. GRα and GRβ proteins were less abundant at the cytoplasmic level in patients (p = 0.048 and 0.005, respectively). The nuclear score of FKBP5 was downregulated in patients (p = 0.028). Moreover, our results revealed that the rs1360780 > T allele is a risk factor to the endemic PF form. This study reported for the first-time the involvement of GRα, GRβ, FKBP5, FKBP4, HAT1 and HDAC2 in PF disease in Tunisian population. - Source: PubMed
Publication date: 2025/02/23
Tahri SafaFakhfakh RaouiaBahloul EmnaCharfi SlimSellami KhadijaHachicha HendBoudawara TahyaTurki HamidaMasmoudi HatemAbida Olfa