Ask about this productRelated genes to: SH3GL2 antibody
- Gene:
- SH3GL2 NIH gene
- Name:
- SH3 domain containing GRB2 like 2, endophilin A1
- Previous symbol:
- -
- Synonyms:
- SH3P4, SH3D2A, CNSA2, EEN-B1
- Chromosome:
- 9p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2016-10-05
Related products to: SH3GL2 antibody
Related articles to: SH3GL2 antibody
- - Source: PubMed
Sinha SatyabrataChunder NeelanjanaMukherjee NupurAlam NeyazRoy AnupRoychoudhury SusantaPanda Chinmay Kumar - Cervical cancer (CC) is an alarming global health problem, with predominantly higher incidence, lethal progression, and mortality among women of African ancestry (AA) than women of European ancestry (EA). Although persistent high-risk human papillomavirus (HPV) integration and infection are the key etiological factors, currently available evidence implicates epigenetic reprogramming as a prime contributor to ancestry-associated differences in CC pathogenesis. To address these disparities, we performed genome-wide DNA methylation profiling of HPV-positive cervical intraepithelial neoplasia (CIN) lesions from AA ( = 15) and EA ( = 15) women. Differential methylation analysis identified a distinct epigenomic landscape in AA-CIN lesions, with widespread hypermethylation and hypomethylation at promoter-associated and regulatory CpG sites. Pathway enrichment analyses highlighted dysregulation of ECM-receptor interaction, focal adhesion, PI3K-Akt, MAPK, Ras, Rap1, and RUNX-dependent transcriptional networks. Comparative analysis across CIN grades (CIN1-CIN3) revealed progressive epigenetic reprogramming affecting cell cycles, cytoskeletal dynamics, signaling, and metabolic pathways. Among hypermethylated tumor suppressor genes, and showed significantly higher methylation in AA lesions, accompanied by concomitant loss of their protein expression. MBD1, a methylation-binding regulator, was upregulated in AA-CIN lesions, coinciding with global loss of 5-hydroxymethylcytosine (5hmC), suggesting enhanced transcriptional repression. In contrast, EA lesions retained protein expression and 5hmC levels. Collectively, these findings indicate that early, ancestry-specific epigenetic modifications target tumor suppressor pathways and converge on oncogenic signaling, cytoskeletal remodeling, and cell-cell adhesion. Our study provides mechanistic insight into CC health disparities, identifying and hypermethylation as potential biomarkers, and highlighting epigenetic regulation as a contributor to disparate CC progression in AA women. - Source: PubMed
Publication date: 2026/04/29
Masoud MohamedShastri CharuBanerjee RajarshiDasgupta SaanviChavarria-Bernal HectorSingh Karan PPierce Jennifer YDasgupta Santanu - The escalating prevalence of diabetes-depression comorbidity (DDC) necessitates novel therapies targeting shared pathophysiological pathways, which needs to decipher the underlying molecular mechanisms. This study elucidates the therapeutic potential of chrysophanol, a natural anthraquinone, in streptozotocin (STZ) and chronic unpredictable mild stress (CUMS)-induced DDC rat model. Behavioral assessments, biochemical profiling, and integrated multi-omics analyses (RNA-seq and proteomics) were employed to decipher underlying mechanisms. Successful model establishment was confirmed by prolonged immobility time in the tail suspension test (p < 0.01) and reduced general health scores. Chrysophanol treatment restored serum brain-derived neurotrophic factor (BDNF) levels (p < 0.01) and ameliorated dyslipidemia (total cholesterol: p < 0.05). RNA-seq results revealed that chrysophanol regulated expression of hundreds of genes, which were enriched in synaptic vesicle cycling (downregulation of Sh3gl2, Camk5), CNS myelination, and axonal ensheathment pathways. Proteomic profile demonstrated the suppression of neurodegenerative markers and activation of axonal regeneration pathways. Notably, chrysophanol downregulated synaptic proteins associated with leukocyte chemotaxis (Pla2g7, Mdk) and glutamatergic synapses (Itpr2, Slc1a1) while upregulated axonal development, regeneration, and PPARγ signaling proteins (Apoa4, Apoa1, Apod), suggesting anti-inflammatory effects and disease-modifying potential through synaptic/axonal regulation. Integrated multi-omics identified overlapping targets linked to neuronal repair (Ankrd27) and iron metabolism (Fth1). These findings suggest chrysophanol as a multitarget agent alleviating DDC via synergistic restoration of neuroplasticity, suppression of neuroinflammation, and rebalancing of metabolic homeostasis, implying a mechanistic foundation for developing chrysophanol-based therapies of diabetes-associated neuropsychiatric disorders. - Source: PubMed
Publication date: 2025/11/28
Hu Xue-JianGe DanMa Xiao-LanYang Yan - Endophilin A, a family of Bin-Amphoterisin-Rvs (BAR) domain-conserved proteins, is found in several tissues and is associated with disease pathogenesis. In patients with breast cancer, endophilin A expression pertains to boosted tumour cell endocytosis, migration, and invadopodia formation, potentially linked to a poor prognosis. - Source: PubMed
Publication date: 2025/10/08
Mehta VikrantIslam SohidulKasana HaritChander Harish - Genetic variants can affect signaling pathways that are important in the pathophysiology of Parkinson's disease (PD). Comprehending their relationship is crucial for the development of diagnostic instruments and preventative drugs for PD. We thoroughly analyzed data from 68 genome-wide association studies to uncover significant genetic variations and clarify the molecular pathways underlying the etiology of Parkinson's disease (PD) resulting from genetic variants. Six common biomarkers linked to PD were found in all 68 investigations: SNCA, TMEM175, BST1, RIT2, LRRK2, and MCCC1. SNCA (↑rs5019538 and ↑rs356182), LRRK2 (↑rs34637584 and ↑rs76904798), and SH3GL2 (↑rs10756907 and ↓rs13294100) were the main biomarkers associated with PD. The clinical traits of PD, such as age at onset, cognitive progression, motor progression, composite progression, tremor dominant, and postural instability gait difficulty, have been found to be underpinned by additional biomarkers, including APOE, NTRK2, SLCO1B3, SLC28A3, AQP10, SNCAIP, ANO2, CADM1, PTPRD, GPR32, GPR321, SQOR, SULT1C2, GABRG2, CYP4Z1, CDH13, and FANCF. Significant evidence was found linking genetic variants linked to an increased risk of PD to reduced dopamine production, receptor recycling, oxidoreductase activity, and increased amyloid-beta accumulation. Considerable evidence links genetic variations with a lower risk of PD due to improved synaptic vesicle signaling, neuron projection development, controlled histone methylation, and excitatory postsynaptic potential. Additionally, we found MYT1L and hsa-miR-20a-5p, which are essential for understanding the genetic variations linked to PD. These findings provide a solid underpinning for future therapeutic approaches aimed at PD, with a focus on the genetic variants and processes connected to the illness. - Source: PubMed
Publication date: 2025/09/30
Nguyen Hai Duc