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Last update 08 May 2025

CRTC3

Last update 08 May 2025

Basic Info

Synonyms

CREB regulated transcription coactivator 3, CREB-regulated transcription coactivator 3, CRTC3

+ [5]

Introduction

Transcriptional coactivator for CREB1 which activates transcription through both consensus and variant cAMP response element (CRE) sites. Acts as a coactivator, in the SIK/TORC signaling pathway, being active when dephosphorylated and acts independently of CREB1 'Ser-133' phosphorylation. Enhances the interaction of CREB1 with TAF4. Regulates the expression of specific CREB-activated genes such as the steroidogenic gene, StAR. Potent coactivator of PPARGC1A and inducer of mitochondrial biogenesis in muscle cells. Also coactivator for TAX activation of the human T-cell leukemia virus type 1 (HTLV-1) long terminal repeats (LTR).

Drugs associated with CRTC3

CN117603969

Patent Mining

Target

CRTC3

Mechanism-

Active Org.

Yueyang Hospital

Originator Org.

Yueyang Hospital

Active Indication

Liver Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CRTC3

100 Translational Medicine associated with CRTC3

0 Patents (Medical) associated with CRTC3

110

Literatures (Medical) associated with CRTC3

01 Jul 2025·Modern Pathology

RNA In Situ Hybridization Detection of CRTC1/3::MAML2 Fusions and LINC00473 in Mucoepidermoid Carcinomas and Hidradenomas of Breast, Salivary Glands, and Skin

Article

Author: Bishop, Justin A ; Krings, Gregor ; Chen, Yunn-Yi ; Bremer, Ryan ; Bean, Gregory R ; Rutland, Cooper D ; Bridge, Julia A ; Wang, Aihui ; Kingsley, Leandra ; Zdravkovic, Sabrina ; Laser, Jordan S ; Das, Ishani

Genomic rearrangements involving MAML2 have been reported in mucoepidermoid carcinoma (MEC) arising in various anatomical sites, as well as the benign counterpart of hidradenoma (HA). Depending on the location, MAML2-rearranged neoplasms may share morphologic overlap with additional diagnostic entities, including other salivary gland malignancies and cutaneous mimics. In some cases, detection of a CRTC1::MAML2 or less common CRTC3::MAML2 rearrangement by fluorescence in situ hybridization (ISH) or next-generation sequencing may be necessary to help confirm the diagnosis. However, such testing can be time consuming, relatively expensive, and unavailable in many pathology laboratories. We describe the development and validation of an ISH custom BaseScope assay targeting the recurrent breakpoints of CRTC1::MAML2 and CRTC3::MAML2 rearrangements. Moreover, we investigated the diagnostic utility of LINC00473 RNAscope as a surrogate marker for MAML2 fusion status. LINC00473 is a long noncoding RNA reportedly downstream of the CRTC1::MAML2 oncoprotein. We evaluated 227 patient cases, including 30 salivary gland and 2 breast MEC, 14 cutaneous and 8 breast HA, and 173 cases representing >20 potential histologic entities in the differential diagnosis for the presence of each fusion transcript by BaseScope, and a subset of cases (n = 205) for the detection of LINC00473 by RNAscope. RNA ISH was directly visualized by chromogenic signal, and the MAML2 fusion partner could be positively identified in the majority of cases. Overall, RNA ISH demonstrates high concordance with orthogonal testing, with CRTC1/3::MAML2 BaseScope showing 93% sensitivity and 100% specificity and LINC00473 RNAscope showing 92% sensitivity and 99% specificity. RNA ISH for CRTC1/3::MAML2 rearrangements and LINC00473 represent reasonable timely and cost-effective alternatives to fluorescence ISH and next-generation sequencing. Such markers may provide the means for accurate diagnosis to ensure appropriate therapy of MEC and HA-neoplasms that can arise in multiple anatomical sites and be encountered by a wide range of pathologists.

01 Apr 2025·Journal of Cutaneous Pathology

Genomic and Transcriptomic Profiling of Digital Papillary Adenocarcinomas Reveals Alterations in Matrix Remodeling and Metabolic Genes

Article

Author: Nagarajan, Priyadharsini ; Vasudevaraja, Varshini ; Shen, Guomiao ; Torres‐Cabala, Carlos A. ; Lai, Zongshan ; Bayraktar, Erol Can ; Ivan, Doina ; Curry, Jonathan L. ; Chiriboga, Luis ; Prieto, Victor G. ; Gill, Pavandeep ; Jour, George ; Aung, Phyu P.

ABSTRACTBackgroundDigital papillary adenocarcinoma (DPAC) is a rare but aggressive cutaneous malignant sweat gland neoplasm that occurs on acral sites. Despite its clinical significance, the cellular and genetic characteristics of DPAC remain incompletely understood.MethodsWe conducted a comprehensive genomic and transcriptomic analysis of DPAC (n = 14) using targeted next‐generation DNA and RNA sequencing, along with gene expression profiling employing the Nanostring Technologies nCounter IO 360 Panel. Gene expression in DPAC was compared to that in hidradenoma (n = 10). Immunohistochemistry was employed to validate gene expression.ResultsTwo out of eight DPACs showed fusion gene rearrangements (CRTC3::MAML2 and TRPS1::PLAG1). No uniform mutational signature was detected in DPAC. Comparative gene expression analysis revealed an enrichment of genes related to matrix remodeling, metabolism, and DNA damage repair. Hallmark pathway analysis demonstrated significant upregulation of E2F target genes in DPAC compared to hidradenoma (p = 0.00710). Human papillomavirus‐42 was found to be positive in all of our tested DPAC cases. Immunohistochemistry confirmed increased protein expression of CD56, CDC20, and SOX10 in DPAC. Notably, most DPAC tumors also exhibited B‐cell infiltration, as indicated by CD20 staining.ConclusionsOur findings reveal novel fusions and validate altered replication pathways related to HPV42 in DPAC.

01 Feb 2025·Virologica Sinica

CRTC3 restricts SARS-CoV-2 replication and is antagonized by CREB

Article

Author: Luo, Rong-Hua ; Long, Xin-Yan ; Cheng, Wei ; Fu, Xiang-Hui ; Zeng, Xiao-Tao ; Ren, Hai-Yan ; Tang, Ying ; Zheng, Yong-Tang ; Zhang, Wan-Jiang ; Yang, Li ; Ren, Si-Xue

Virus-encoding RNA-dependent RNA polymerase (RdRp) is essential for genome replication and gene transcription of human coronaviruses (HCoVs), including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We previously identified the interaction between the catalytic subunit NSP12 of SARS-CoV-2 RdRp and the host protein CREB-regulated transcription coactivator 3 (CRTC3), a member of the CRTC family that regulates cyclic AMP response element-binding protein (CREB)-mediated transcriptional activation. Currently, the implication of CRTC3 in the pathogenesis of HCoVs is poorly understood. Herein, we demonstrated that CRTC3 attenuates RdRp activity and SARS-CoV-2 genome replication, therefore reducing the production of progeny viruses. The interaction of CRTC3 with NSP12 contributes to its inhibitory effect on RdRp activity. Furthermore, we expanded the suppressive effects of two other CRTC family members (CRTC1 and CRTC2) on the RdRp activities of lethal HCoVs, including SARS-CoV-2 and Middle East respiratory syndrome coronavirus (MERS-CoV), along with the CREB antagonization. Overall, our research suggests that CRTCs restrict the replication of HCoVs and are antagonized by CREB, which not only provides new insights into the replication regulation of HCoVs, but also offers important information for the development of anti-HCoV interventions.

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