Ask about this productRelated genes to: CREB5 antibody
- Gene:
- CREB5 NIH gene
- Name:
- cAMP responsive element binding protein 5
- Previous symbol:
- -
- Synonyms:
- H_GS165L15.1, CRE-BPA
- Chromosome:
- 7p15.1-p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-04
- Date modifiied:
- 2018-02-13
Related products to: CREB5 antibody
Related articles to: CREB5 antibody
- Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide. The identification of effective molecular targets is crucial for advancing precision medicine and prognostic strategies. This study aims to uncover key CRC biomarkers through integrative bioinformatics analyses, providing mechanistic insights for therapeutic development. - Source: PubMed
Publication date: 2026/04/14
Pu GenyuanYin ZiZhang XinLiu ZhiqiYang CaitingXu ChunpingLai Mingming - Transient cell states that precede and support human myogenic lineage commitment, and the intrinsic and extrinsic signals that control them, remain poorly defined in vitro. Here, we used longitudinal single-nucleus profiling, together with a SIX1:H2B-GFP hPSC reporter for lineage tracing, resolved previously uncaptured transient intermediates and sequential waves of human myogenesis across differentiation and . We show that hPSC-directed myogenesis gives rise in parallel to paraxial mesoderm and a transient PAX8+ intermediate mesoderm population that forms a 3-dimensional pre-myogenic niche supporting the PAX3-to-PAX7 myogenic progenitor transition. LIANA+ analysis further identified a temporally restricted BMP7-BMPR1B interaction, together with laminin-linked signaling, between PAX8+ niche cells and skeletal muscle progenitors before commitment. We further show that dynamic SIX1 cofactor switching, including EYA3 activity, is required for PAX3-to-PAX7 progression, and that disruption of this program compromises multi-lineage niche integrity. Together, these findings define how transient niche populations and intrinsic regulatory networks coordinate early human myogenic lineage progression and provide a human in vitro platform to study parallel intermediate and paraxial mesoderm development during myogenesis. - Source: PubMed
Publication date: 2026/03/31
Jaime Olga GBazan Katherine FLi AngelaDeai Asja ALakatos AnitaHicks Michael R - Copyright: © 2026 Makovec et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Prostate gland cells can be transcriptionally and morphologically characterized as basal and luminal. About 30–40% of advanced prostate cancers (PC) harbor basal-like transcription programs. In castration-resistant PC (CRPC), studies indicate that basal and stem cell-like (SCL) tumors are major resistance mechanisms to androgen receptor (AR)-targeted therapies. SCL tumors have reduced AR activity and increased stem-cell activity that promotes tumor formation, which contributes to poor clinical outcomes. We determined that CREB5 is a key regulator of basal and SCL transcriptional programs and tumor-forming phenotypes in PC. Through in silico modeling of PC transcriptomes and several pre-defined PC signaling programs, CREB5 expression was best associated with basal-like gene signatures and SCL-associated genes in primary PC and CRPCs (n = 493 and 208). This included associations with FOSL1 and other AP-1 transcription factors. We further found that CREB5 interacted with AP-1 proteins and bound to the regulatory elements of AP-1 genes, suggesting a mechanistic role in regulating the activity of AP-1 genes. In AR-positive cells, CREB5 overexpression promoted cell colony growth with tumorigenic properties and increased tumor size in vivo. These findings implicate CREB5 as a driver of the transcriptional programs underlying AR-independent basal and SCL CRPC subtypes, and this activity is detectable in primary PC. - Source: PubMed
Publication date: 2026/03/17
Makovec AllisonPhoenix John TBergom Hannah EBoytim EllaGustafson Ava PDeacon AidenTape SydneyAli AtefLudwig MeganPitzen Samuel PMoline DavidRichter CamdenLongie HudsonSu Mei-ChiJena SampreetiLikasitwatanakul PornladaDrake Justin MHuang R StephanieHahn William CRennhack Jonathan PDehm Scott MKregel StevenAntonarakis Emmanuel SHwang Justin - Temporomandibular joint (TMJ) plays critical roles in the movement of mandible. TMJ osteoarthritis (TMJOA) leads to pain and limited jaw function. Histologically, TMJOA causes cartilage degradation and a reduction in extracellular matrix (ECM) stiffness. The superficial zone chondrocytes (SZC) contribute in the regeneration of the condylar fibrocartilage in TMJ, while their responses to the softened ECM remains unclear. Here, we showed that the ECM stiffness was decreased in the superficial zone cartilage of TMJOA patients and rat models. Single-cell RNA sequencing demonstrated the diminished phospholipid phosphatase 3 (Plpp3) expression, impaired migration, and ECM secretion, as well as the down-regulated PI3K-AKT pathway of SZC in rat TMJOA. Such alternations were also revealed by mRNA sequencing of SZC cultured on the softened ECM. Further studies disclosed that reduced ECM stiffness induced decreased PLPP3 on the endoplasmic reticulum (ER), which inhibited mitochondrial fission and respiration via increasing phosphatidic acid (PA) in the mitochondria. Meanwhile, deactivated PI3K-AKT pathway reduced the intra-nuclear translocation of transcriptional factor Cyclic AMP responsive element binding protein 5 (CREB5), which limited PLPP3 expression. Overexpression of PLPP3 alleviated the functional damage of SZC in vitro and the cartilage ECM degradation in vivo. This work displayed the functional impairment of SZC on the softened ECM and the underlying mechanism, as well as suggested PLPP3 as a potential target in the regenerative treatments for TMJOA. - Source: PubMed
Publication date: 2026/03/23
Yu YekeWen DongshengZou LuxiangZhu HuiminZhang XiaoyuWang ChuandongLu ChuanZhao JieyunZhang YifanHe DongmeiZhang Zhiyuan - Intervertebral disc degeneration (IDD) is a major contributor to low back pain (LBP), with ferroptosis recently recognized as a key mechanism underlying its progression.This study investigates the protective role of cAMP response element-binding protein 5 (CREB5) in IDD, focusing on its capacity to preserve extracellular matrix (ECM) integrity and to modulate ferroptosis and mitochondrial oxidative stress through activation of the NR4A1-PGC-1α signaling axis. - Source: PubMed
Publication date: 2026/03/17
Huang YehengXiao BingruLiang HaiboZhu YuxuanYang ShuLi SunlongShi YifengWang XueqiangWang Xiangyang