CREB1 (phospho-Ser142) Antibody
- Known as:
- CREB1 (phosphorilated-Ser142) Antibody
- Catalog number:
- abx000382
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- CREB1 (phospho-Ser142) Antibody
Related genes to: CREB1 (phospho-Ser142) Antibody
- Gene:
- CREB1 NIH gene
- Name:
- cAMP responsive element binding protein 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-02-05
- Date modifiied:
- 2016-10-05
Related products to: CREB1 (phospho-Ser142) Antibody
Related articles to: CREB1 (phospho-Ser142) Antibody
- Cognitive decline is a hallmark of neurodegenerative diseases. The complex pathophysiology of these diseases has limited the efficacy of current therapies. The co-administration of epidermal growth factor (EGF) and growth hormone-releasing peptide 6 (GHRP6) emerges as a promising neuroprotective candidate. The present study evaluated the therapeutic potential of this combination in two preclinical models of cognitive impairment: (i) age-related decline and (ii) impairment induced by intracerebroventricular administration of streptozotocin (STZ). In both experiments, C57BL/6 mice were used and distributed into three experimental groups, each comprising 14-15 animals per group. Cognitive and motor function was assessed through gait pattern, Y-maze and novel object recognition tests. Differential gene expression was analyzed using qPCR. Both models reproduced hallmark features of cognitive decline, including deficits in working and spatial memory and changes in the expression of genes associated with oxidative stress, neuroinflammation and synaptic plasticity. In aged animals, EGF + GHRP6 treatment increased step length (p = 0.04). In the forced alternation Y-maze test, aged-EGF + GHRP6 animals made more visits to the novel arm than to the familiar arm 1 (p = 0.001) or to the familiar arm 2 (p = 0.04). Cognitive benefits were also observed in the STZ-induced model. STZ-EGF + GHRP6 group exhibited an alternation percentage higher than the STZ-vehicle group (p = 0.03). Moreover, EGF + GHRP6 treatment significantly increased the expression of genes associated with antioxidant defense (Hmox1), synaptic plasticity (Creb1), and oligodendrocyte differentiation (Olig1) while concurrently reducing the expression of Nfkb1. These findings highlight the therapeutic potential of EGF + GHRP6 co-administration as a neuroprotective strategy to mitigate neurodegeneration and preserve cognitive function. - Source: PubMed
Publication date: 2026/07/04
Risco-Acevedo DanielaSubirós-Martínez NelvysCamacho-Rodríguez HanletRamírez-Sánchez JeneyRodríguez-Virulich YaimaEtchegoyen-Amoros Ana YansiHernández-Estrada WendyWong-Guerra MaylinMontano-Peguero YanayEstrada-Olivares ThaliaFuentes-Morales DashaPalenzuela-Gardón DanielPérez-Saad HéctorNúñez-Figueredo YanierWen LiGuillén-Nieto Gerardo EGarcía-Del-Barco-Herrera Diana - This study aimed to investigate whether miR-425-5p contributes to post-spinal cord injury (SCI) inflammation and motor dysfunction by targeting CREB1. - Source: PubMed
Publication date: 2026/06/26
Qi SinaWang DaweiWu YingshuangWang WeizhongWang SimengMeng HeZhang ZheLuo YiWang Xiaona - BackgroundGastric cancer (GC) is a highly prevalent malignant tumor worldwide. Traditional treatment approaches have numerous limitations, and messenger RNA (mRNA)-targeted therapy offers a new direction for the treatment of GC.ObjectiveTo investigate the expression characteristics and clinical significance of miR-145-3p in GC, as well as its mechanism of action in regulating GC cell function by targeting CREB1.MethodsQuantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-145-3p and CREB1 in GC tissues, serum, and cell lines. Cell Counting Kit-8, Transwell, and qRT-PCR assays were employed to evaluate the effects of miR-145-3p and CREB1 on GC cell proliferation, migration, invasion, and apoptosis. Bioinformatics prediction, dual-luciferase reporter assays, and rescue experiments were conducted to validate the targeted regulatory relationship between miR-145-3p and CREB1. Downstream signaling pathways were analyzed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses.ResultsmiR-145-3p is significantly downregulated in GC, which is closely linked with tumor malignant progression and negative prognosis. miR-145-3p mimic inhibits the proliferation, migration, and invasion of GC cells while promoting apoptosis; conversely, CREB1 OE produces the opposite effect. Bioinformatics and functional experiments confirmed that miR-145-3p targets CREB1, and CREB1 OE partially reverses the tumor-suppressive effects of miR-145-3p. GO and KEGG analyses revealed that the miR-145-3p/CREB1 axis participates in transcription regulation, metabolism, and virus-related carcinogenesis pathways.ConclusionmiR-145-3p exerts effects in GC, at least in part, by targeting and inhibiting CREB1, positioning it as a potential molecular target for GC diagnosis, prognosis assessment, and mRNA-targeted therapy. - Source: PubMed
Publication date: 2026/07/03
Yao KaitaoZhu YanZhang Bing - Obesity, a major global health challenge associated with metabolic and cardiovascular disorders, has drawn increasing attention to the therapeutic potential of white adipose tissue (WAT) browning. Although the lysine methyltransferase SETD7 has been implicated in various cardiovascular and metabolic diseases, its role in adipose thermogenesis remains unclear. Here, we reported that SETD7 was upregulated in inguinal WAT (iWAT) of obese mice and was primarily localized to mature adipocytes. Setd7 knockdown (Setd7) mice exhibited enhanced thermogenic gene expression and iWAT browning upon cold exposure or β3-adrenergic stimulation, whereas thermogenic activity in brown adipose tissue (BAT) remained largely unaffected. In vitro, SETD7 knockdown did not alter adipogenesis but potently augmented thermogenic capacity in beige adipocytes, while SETD7 overexpression exerted the opposite effect. Mechanistically, RNA-Seq analysis revealed that SETD7 deficiency upregulated Adcy7 transcription, leading to increased Sirt1 levels and enhanced Creb1 phosphorylation, thereby activating the thermogenic program. Notably, Setd7 mice resisted high-fat diet (HFD)-induced obesity, exhibiting reduced weight gain, elevated energy expenditure, and improved metabolic health. Together, these findings identify SETD7 as a negative regulator of iWAT thermogenesis and suggest that targeting SETD7 may represent a promising strategy for combating obesity. - Source: PubMed
Publication date: 2026/07/01
Xiao ChenxiHu YajieLiu JiayaoZhao JialinXu JieChen HonghongHuang QiuyuanChen WuguiChang JunLiu XinhuaLin Chengshou - Osteosarcoma (OS) remains a clinically challenging primary bone tumor because of its strong metastatic potential and unsatisfactory outcomes in advanced cases. Parathyroid hormone receptor 1 (PTHR1), a receptor closely associated with bone-related signaling, has not been fully characterized in OS. This study explored whether PTHR1 contributes to OS progression and clarified the downstream regulatory mechanism involved. - Source: PubMed
Publication date: 2026/06/29
Zhang JiamingLi WeishangLiu FeiZhang HuiWang Wei