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Last update 08 May 2025

SYT2

Last update 08 May 2025

Basic Info

Synonyms

synaptotagmin 2, Synaptotagmin II, Synaptotagmin-2

+ [2]

Introduction

Exhibits calcium-dependent phospholipid and inositol polyphosphate binding properties (By similarity). May have a regulatory role in the membrane interactions during trafficking of synaptic vesicles at the active zone of the synapse (By similarity). Plays a role in dendrite formation by melanocytes (PubMed:23999003).

Drugs associated with SYT2

Exo-1

Target

SYT2

Mechanism

SYT2 inhibitors

Active Org.

Exotect, LLC

Originator Org.

Exotect, LLC

Active Indication

Respiration Disorders

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SYT2

100 Translational Medicine associated with SYT2

0 Patents (Medical) associated with SYT2

213

Literatures (Medical) associated with SYT2

01 Mar 2025·Journal of Genetic Engineering and Biotechnology

Exploration of crucial stromal risk genes associated with prognostic significance and chemotherapeutic opportunities in invasive ductal breast carcinoma

Article

Author: Tang, Guohua ; Zhang, Yang ; Geng, Wei ; Yu, Yang ; Wang, Zhi

BACKGROUNDFew studies revealed that stromal genes regulate the tumor microenvironment (TME). However, identification of key-risk genes in the invasive ductal breast carcinoma-associated stroma (IDBCS) and their associations with the prediction of risk group remains lacking.METHODSThis study used the GSE9014, GSE10797, GSE8977, GSE33692, and TGGA BRCA datasets. We explored the differentially expressed transcriptional markers, hub genes, gene modules, and enriched KEGG pathways. We employed a variety of algorithms, such as the log-rank test, the LASSO-cox model, the univariate regression model, and the multivariate regression model, to predict prognostic-risk genes and the prognostic-risk model. Finally, we employed a molecular docking-based study to explore the interaction of sensitive drugs with prognostic-risk genes.RESULTSIn comparing IDBCS and normal stroma, we discovered 1472 upregulated genes and 1400 downregulated genes (combined ES > 0585 and adjusted p-value < 0.05). The hub genes enrich cancer, immunity, and cellular signaling pathways. We explored the 12 key risk genes (ADAM8, CD86, CSRP1, DCTN2, EPHA1, GALNT10, IGFBP6, MIA, MMP11, RBM22, SLC39A4, and SYT2) in the IDBCS to identify the high-risk group and low-risk group patients. The high-risk group had a lower survival rate, and the constructed ROC curves evaluated the validity of the risk model. Expression validation and diagnostic efficacy revealed that the key stromal risk genes are consistently deregulated in the high-risk group and high stromal samples of the TCGA BRCA cohort. The expression of crucial risk genes, including CD86, CSRP1, EPHA1, GALNT10, IGFBP6, MIA, and RBM22 are associated with drug resistance and drug sensitivity. Finally, a molecular docking study explored several sensitive drugs (such as QL-XII-61, THZ-2-49, AZ628, NG-25, lapatinib, dasatinib, SB590885, and dabrafenib) interacted with these essential risk genes through hydrogen bonds and other chemical interactions.CONCLUSIONSExploring essential prognostic-risk genes and their association with the prognosis, diagnostic efficacy, and risk-group prediction may provide substantial clues for targeting the breast cancer stromal key-risk genes.

01 Feb 2025·CNS Neuroscience & Therapeutics

Discovery of Novel Pain Regulators Through Integration of Cross‐Species High‐Throughput Data

Article

Author: Ruan, Junpu ; Chen, Gang ; Xiang, Jiahui ; Li, Nan ; Chen, Ying ; Lu, Lu ; Bajpai, Akhilesh K. ; Zhang, Ran ; Wang, Angelina ; Gu, Qingqing

ABSTRACTAimsChronic pain is an impeding condition that affects day‐to‐day life and poses a substantial economic burden, surpassing many other health conditions. This study employs a cross‐species integrated approach to uncover novel pain mediators/regulators.MethodsWe used weighted gene coexpression network analysis to identify pain‐enriched gene module. Functional analysis and protein‐protein interaction (PPI) network analysis of the module genes were conducted. RNA sequencing compared pain model and control mice. PheWAS was performed to link genes to pain‐related GWAS traits. Finally, candidates were prioritized based on node degree, differential expression, GWAS associations, and phenotype correlations.ResultsA gene module significantly over‐enriched with the pain reference set was identified (referred to as “pain module”). Analysis revealed 141 pain module genes interacting with 46 pain reference genes in the PPI network, which included 88 differentially expressed genes. PheWAS analysis linked 53 of these genes to pain‐related GWAS traits. Expression correlation analysis identified Vdac1, Add2, Syt2, and Syt4 as significantly correlated with pain phenotypes across eight brain regions. NCAM1, VAMP2, SYT2, ADD2, and KCND3 were identified as top pain response/regulator genes.ConclusionThe identified genes and molecular mechanisms may enhance understanding of pain pathways and contribute to better drug target identification.

01 Jan 2025·Neurotherapeutics

IGF-1 impacts neocortical interneuron connectivity in epileptic spasm generation and resolution

Article

Author: Le, John T ; Ballester-Rosado, Carlos J. ; Lam, Trang T. ; Le, John T. ; Frost, James D. ; Ballester-Rosado, Carlos J ; Anderson, Anne E. ; Swann, John W. ; Anderson, Anne E ; Swann, John W ; Lam, Trang T ; Frost, James D

Little is known about the mechanisms that generate epileptic spasms following perinatal brain injury. Recent studies have implicated reduced levels of Insulin-like Growth Factor 1 (IGF-1) in these patients' brains. Other studies have reported low levels of the inhibitory neurotransmitter, GABA. In the TTX brain injury model of epileptic spasms, we undertook experiments to evaluate the impact of IGF-1 deficiencies on neocortical interneurons and their role in spasms. Quantitative immunohistochemical analyses revealed that neocortical interneurons that express glutamic acid decarboxylase, parvalbumin, or synaptotagmin 2 co-express IGF-1. In epileptic rats, expression of these three interneuron markers were reduced in the neocortex. IGF-1 expression was also reduced, but surprisingly this loss was confined to interneurons. Interneuron connectivity was reduced in tandem with IGF-1 deficiencies. Similar changes were observed in surgically resected neocortex from infantile epileptic spasms syndrome (IESS) patients. To evaluate the impact of IGF-1 deficiencies on interneuron development, IGF-1R levels were reduced in the neocortex of neonatal conditional IGF-1R knock out mice by viral injections. Four weeks later, this experimental maneuver resulted in similar reductions in interneuron connectivity. Treatment with the IGF-1 derived tripeptide, (1-3)IGF-1, abolished epileptic spasms in most animals, rescued interneuron connectivity, and restored neocortical levels of IGF-1. Our results implicate interneuron IGF-1 deficiencies, possibly impaired autocrine IGF-1 signaling and a resultant interneuron dysmaturation in epileptic spasm generation. By restoring IGF-1 levels, (1-3)IGF-1 likely suppresses spasms by rescuing interneuron connectivity. Results point to (1-3)IGF-1 and its analogues as potential novel disease-modifying therapies for this neurodevelopmental disorder.

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