Last update 19 Sep 2024

CREB1

Last update 19 Sep 2024

Basic Info

Synonyms

cAMP responsive element binding protein 1, cAMP-responsive element-binding protein 1, CREB-1

+ [2]

Introduction

Phosphorylation-dependent transcription factor that stimulates transcription upon binding to the DNA cAMP response element (CRE), a sequence present in many viral and cellular promoters. Transcription activation is enhanced by the TORC coactivators which act independently of Ser-119 phosphorylation. Involved in different cellular processes including the synchronization of circadian rhythmicity and the differentiation of adipose cells.

Drugs associated with CREB1

FT-1050 treated UCB

Target

CREB1

Mechanism

CREB1 agonists

Active Org.-

Originator Org.

Mass General Brigham, Inc.

Active Indication-

Inactive Indication

Acute Lymphoblastic Leukemia [+5]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with CREB1

NCT02354443 / TerminatedPhase 1

A Phase 1 Trial of a Single ProHema® CB Product as Part of Single Cord Blood Unit Transplant After Busulfan/Cyclophosphamide/ATG Conditioning for Pediatric Patients With Inherited Metabolic Disorders

The purpose of this study is to describe the safety profile of ProHema-CB as part of a single cord blood unit transplant after a myeloablative conditioning regimen in pediatric patients with inherited metabolic disorders. The safety profile will primarily be assessed by neutrophil engraftment.

Start Date01 Jun 2015

Sponsor / Collaborator

Fate Therapeutics, Inc.

NCT01627314 / TerminatedPhase 2

A Phase 2 Controlled Trial of a Single ProHema®-CB Unit (Ex Vivo Modulated Human Cord Blood) As Part of a Double Umbilical Cord Blood Transplant Following Myeloablative or Reduced Intensity Conditioning For Patients Age 15-65 Years With Hematologic Malignancies.

This study is an open-label randomized, prospectively and historically controlled trial of the safety and efficacy of a single ProHema-CB unit used as part of a double CB transplant following myeloablative or reduced intensity conditioning for subjects age 15-65 years with hematologic malignancies. A maximum of 60 eligible subjects will be enrolled and treated in the trial at approximately 10 centers within the U.S.

Start Date01 Jul 2012

Sponsor / Collaborator

Fate Therapeutics, Inc.

NCT01527838 / CompletedPhase 1

A Phase I Trial of a Single FT1050 (16,16-Dimethyl Prostaglandin E2) Ex Vivo-Modulated Umbilical Cord Blood (CB) Unit Following a Reduced Intensity Conditioning Regimen For Adults With Hematologic Malignancies

This trial is a prospective, open-label, single-arm trial of the safety of a single FT1050-treated CB unit for hematopoietic reconstitution after a reduced-intensity conditioning regimen for hematologic malignancies. A maximum of 40 eligible adult subjects will be enrolled and treated in the trial at approximately 2-4 centers within the U.S.

Start Date01 Jan 2012

Sponsor / Collaborator

Fate Therapeutics, Inc.

100 Clinical Results associated with CREB1

100 Translational Medicine associated with CREB1

0 Patents (Medical) associated with CREB1

2,243

Literatures (Medical) associated with CREB1

05 Jul 2106·Oncotarget

Wnt/β-catenin pathway transactivates microRNA-150 that promotes EMT of colorectal cancer cells by suppressing CREB signaling

Article

Author: Wang, Lu-Qin ; Zhou, Ai-Dong ; Li, Bin ; Zhou, Hui ; Zhang, Yin ; Xu, Hui ; Guo, Yan-Hua ; Xie, Shu-Juan ; Yu, Peng ; Qu, Liang-Hu ; Yang, Jian-Hua ; Zheng, Li-Si ; Zhang, Chen-Min ; Liang, Zi-Rui

A hallmark of aberrant activation of the Wnt/β-catenin signaling pathway has been observed in most colorectal cancers (CRC), but little is known about the role of non-coding RNAs regulated by this pathway. Here, we found that miR-150 was the most significantly upregulated microRNA responsive to elevated of Wnt/β-catenin signaling activity in both HCT116 and HEK293T cells. Mechanistically, the β-catenin/LEF1 complex binds to the conserved TCF/LEF1-binding element in the miR-150 promoter and thereby transactivates its expression. Enforced expression of miR-150 in HCT116 cell line transformed cells into a spindle shape with higher migration and invasion activity. miR-150 markedly suppressed the CREB signaling pathway by targeting its core transcription factors CREB1 and EP300. Knockdown of CREB1 or EP300 and knockout of CREB1 by CRISPR/Cas9 phenocopied the epithelial-mesenchymal transition (EMT) observed in HCT116 cells in response to miR-150 overexpression. In summary, our data indicate that miR-150 is a novel Wnt effector that may significantly enhance EMT of CRC cells by targeting the CREB signaling pathway.

31 Dec 2024·Autoimmunity

Silencing of CircTRIM25/miR-138-5p/CREB1 axis promotes chondrogenesis in osteoarthritis

Article

Author: Zeng, Wanhui ; Zeng, Zhaogan ; Liu, Chenghong ; Liu, Sheng ; He, Chunlei ; Liu, Xunzhi ; Yang, Yadong ; Wu, Qiang ; Ye, Shanshan

BACKGROUNDDysregulated circular RNAs (circRNAs) are involved in osteoarthritis (OA) progression.OBJECTIVEWe aimed to explore the effect of hsa_circ_0044719 (circTRIM25) on the ferroptosis of chondrocytes.METHODSChondrocytes were treated with interleukin (IL)-1β to generate cell model. Cellular behaviours were measured using cell counting kit-8, enzyme-linked immunosorbent assay, relevant kits, propidium iodide staining, and immunofluorescence assay. Quantitative real-time polymerase chain reaction was performed to examine the expression of circTRIM25, miR-138-5p, and cAMP responsive element binding protein 1 (CREB1), and their interactions were assessed using luciferase reporter analysis and RNA pull-down assay.RESULTSCircTRIM25 was upregulated in OA tissues and IL-1β-stimulated chondrocytes. Knockdown of circTRIM25 facilitated the viability and suppressed ferroptosis and inflammation of IL-1β-induced cells. CircTRIM25 served as a sponge of miR-138-5p, which directly targets CREB1. Downregulation of miR-138-5p abrogated the effect induced by knockdown of circTRIM25. Furthermore, enforced CREB1 reversed the miR-138-5p induced effect. Moreover, knockdown of circTRIM25 attenuated cartilage injury in vivo.CONCLUSIONSilencing of circTRIM25 inhibited ferroptosis of chondrocytes via the miR-138-5p/CREB axis and thus attenuated OA progression.

01 Dec 2024·Journal of Ethnopharmacology

Buyang huanwu decoction improves synaptic plasticity of ischemic stroke by regulating the cAMP/PKA/CREB pathway

Article

Author: Gong, Mingyu ; Mo, Jingyuan ; Wang, Pengcheng ; Liao, Weiguo ; Zhong, Lanying ; Du, Jinyan ; Su, Anyu ; Kuang, Huizhen ; Li, Yaxin ; Wang, Lisheng ; Huang, Xiaoling ; Liu, Zai

ETHNOPHARMACOLOGICAL RELEVANCEIschemic stroke is an acute central nervous system disease that poses a threat to human health. It induces a series of severe pathological mechanisms, ultimately leading to neuronal cell death in the brain due to local ischemia and hypoxia. Buyang Huanwu decoction (BYHWD), as a representative formula for treating ischemic stroke, has shown good therapeutic effects in stroke patients.AIM OF THE STUDYThis study aimed to explore the mechanism of BYHWD in promoting neural remodeling after ischemic stroke from the perspective of neuronal synaptic plasticity, based on the cAMP/PKA/CREB signaling pathway.MATERIALS AND METHODSA modified suture technique was employed to establish a rat model of MCAO. The rats were divided into sham, model, and BYHWD (20 g/kg) groups. After the corresponding intervention, rat brains from each group were collected. TMT quantitative proteomics technology was employed for the research. Following proteomics studies, we investigated the mechanism of BYHWD in the intervention of ischemic stroke through animal experiments and cell experiments. The experimental animals were divided into sham, model, and BYHWD (5 g/kg, 10 g/kg, and 20 g/kg) groups. Infarct volume and severity of brain injury were measured by TTC staining. HE staining was utilized to evaluate alterations in tissue morphology. The Golgi staining was used to observe changes in cell body, dendrites, and dendritic spines. Transmission electron microscopy was used to observe the ultrastructure of synapses in the cortex and hippocampus. TUNEL staining was conducted to identify apoptotic neurons. Meanwhile, a stable and reliable (OGD/R) SH-SY5Y cell model was established. The effect of BYHWD-containing serum on SH-SY5Y cell viability was measured by CCK-8 kit. The apoptosis situation of SH-SY5Y cells was determined by Annexin V-FITC/PI. Immunofluorescence was employed to measure the fluorescence intensity of synaptic-related factors Syt1, Psd95, and Syn1. Synaptic plasticity pathways were assessed by using RT-qPCR and Western blot to determine the expression levels of cAMP, Psd95, Prkacb, Creb1/p-Creb1, BDNF, Shank2, Syn1, Syt1, Bcl-2, Bcl-2/Bax mRNA and proteins.RESULTSAfter treatment with BYHWD, notable alterations were detected in the signaling pathways linked to synaptic plasticity and the cAMP signaling pathway-related targets among the intervention targets. This trend of change was also reflected in other bioinformatics analyses, indicating the important role of synaptic plasticity changes before and after modeling and drug intervention. The results of vivo and vitro experiments showed that BYHWD improved local pathological changes, and reduced cerebral infarct volume, and neurological function scores in MCAO rats. It increased dendritic spine density, improved synaptic structural plasticity, and had a certain neuroprotective effect. BYHWD increased the postsynaptic membrane thickness, synaptic interface curvature, and synaptic quantity. 10% BYHWD-containing serum was determined as the optimal concentration for treatment. 10% BYHWD-containing serum significantly reduced the overall apoptotic rate of (OGD/R) SH-SY5Y cells. Immunofluorescence experiments demonstrated that 10% BYHWD-containing serum could improve synaptic plasticity and increase the relative expression levels of synaptic-related proteins Syt1, Psd95, and Syn1. BYHWD and decoction-containing serum upregulated the mRNA and protein expression levels in (OGD/R) SH-SY5Y cells and MCAO rats, suggesting its ability to improve damaged neuronal synaptic plasticity and enhance transmission efficiency, which might be achieved through the regulation of the cAMP/PKA/CREB pathway.CONCLUSIONSThis study may provide a basis for clinical medication by elucidating the underlying experimental evidence for the promotion of neural plasticity after ischemic stroke by BYHWD.

Analysis

Perform a panoramic analysis of this field.

view full example data

Chat with Hiro

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

CREB1

Basic Info

Related

Analysis