Ask about this productRelated genes to: TMEM161B Blocking Peptide
- Gene:
- TMEM161B NIH gene
- Name:
- transmembrane protein 161B
- Previous symbol:
- -
- Synonyms:
- MGC33214
- Chromosome:
- 5q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2006-06-21
- Date modifiied:
- 2014-11-19
Related products to: TMEM161B Blocking Peptide
Related articles to: TMEM161B Blocking Peptide
- Glioblastoma (GBM) is the most lethal and aggressive primary brain tumor in adults. Despite a standard-of-care regimen involving surgical resection, radiotherapy and temozolomide (TMZ), median overall survival typically hovers between 12 and 15 months. This poor prognosis is driven by profound intratumoral heterogeneity, glioma stem cell populations, and an immunosuppressive microenvironment that collectively fuel resistance to traditional apoptosis-centric therapies. Ferroptosis-a form of regulated cell death driven by iron-dependent phospholipid peroxidation and the collapse of antioxidant defenses-has emerged as a compelling alternative for eliminating therapy-refractory GBM cells. This review examines the molecular machinery of ferroptosis in glioma and explores how an additional regulatory layer, noncoding RNAs (ncRNAs), modulates this process. We highlight key experimentally validated axes where microRNAs, long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs) orchestrate iron handling and antioxidant thresholds. These include sensitizers like miR-147a and circLRFN5, which promote iron overload, and resistors like circCDK14 and TMEM161B-AS1, which act as "ferroptosis brakes". Furthermore, we discuss how integrative analyses of TCGA and CGGA cohorts have yielded ferroptosis-related lncRNA signatures that robustly predict patient survival. Finally, we outline the clinical potential of these ncRNAs as biomarkers and therapeutic targets while addressing the delivery challenges, such as the blood-brain barrier, that must be overcome to achieve precision, ferroptosis-oriented GBM therapy. - Source: PubMed
Publication date: 2026/04/14
Seerapu Venkata NAmaresan RajalakshmiGopal Udhayakumar - A mechanistic understanding of neurodevelopment requires us to follow the multiscale processes that connect molecular genetic processes to macroscopic cerebral cortical formations and thence to neurological function. Using MRI of the brain of the ferret, a model organism for studying cortical morphogenesis, we create in vitro physical gel models and in silico numerical simulations of normal brain gyrification. Using observations of genetically manipulated animal models, we identify cerebral cortical thickness and cortical expansion rate as the primary drivers of dysmorphogenesis and demonstrate that in silico models allow us to examine the causes of aberrations in morphology and developmental processes at various stages of cortical ontogenesis. Finally, we explain analogous cortical malformations in human brains, with comparisons with human phenotypes induced by the same genetic defects, providing a unified perspective on brain morphogenesis that is driven proximally by genetic causes and affected mechanically via variations in the geometry of the brain and differential growth of the cortex. - Source: PubMed
Publication date: 2025/12/29
Choi Gary P TLiu ChunziYin SifanSéjourné GabrielleSmith Richard SWalsh Christopher AMahadevan L - Lacking social connectedness is associated with broad morbidity. Yet the underlying mechanisms remain obscures, especially given its entanglement with depressive symptoms. Clarifying whether social connectedness confers unique risk beyond depression can guide clinical care and social infrastructure interventions. - Source: PubMed
Publication date: 2025/11/23
Shao LucyPakala ShreyaXu BohanLoughnan RobertAhern JohnathanZheng HaixiaThompson Wesley KPaulus MartinFan Chun Chieh - Noncoding RNA regulatory networks play crucial roles in human breast cancer. The aim of this study was to establish a network containing multi-type RNAs and RBPs in triple-negative breast cancer (TNBC). Differential expression analyses of lncRNAs, miRNAs, and genes were performed using the GEO2R tool. Downstream RBPs and miRNAs were identified using respective databases. GO, KEGG, and protein-protein interaction were predicted. Expression of mRNAs, lncRNAs, and miRNAs were examined using TCGA and ENCORI. TMEM161B-AS1-miR-3646-SERPINB5 axis was validated with the expression level and cell function. TMEM161B-AS1-RBFOX1-SER-PINB5 axis was validated using RIP assays. A lncRNA-miRNA-mRNA network, a lncRNA-RBP-mRNA network, and a lncRNA-miRNA/RBP-mRNA network were constructed. Alterations in the expression levels of TMEM161B-AS1, miR-3646, and SERPINB5 were confirmed by real-time polymerase chain reaction as downregulation, upregulation, and downregulation, respectively. TMEM161B-AS1 inhibited TNBC cell proliferation, migration, and invasion. miR-3646 reversed the inhibitory effect of TMEM161B-AS1 on cell function, while SERPINB5 offset the miR-3646 effect. RB-FOX1 bound to SERPINB5 mRNAs, and TMEM161B-AS1 was involved in their interaction. This study revealed the ln-cRNA-miRNA/RBP-mRNA network in TNBC, providing more directions to study the molecular mechanism of TNBC. - Source: PubMed
Yun WenLi YaoHuang JianyuanYuan Yuan - Birds are inherently social creatures that rely on pairing to enhance their well-being. Since many bird species lack obvious physical differences between females and males, sex identification is essential for ensuring their welfare. Additionally, early determination of the sexes of birds is crucial for their breeders, especially considering that most companion birds do not display clear sexual characteristics. Molecular genetic sexing has been demonstrated to be the most reliable method for determining the sexes of monomorphic birds. The objective of the present study was to demonstrate rapid, effective, and precise identification of sex in birds through quantitative real-time PCR (qPCR) using samples obtained via a minimally invasive technique (oral swabs). This qPCR method assesses variations in gene copy numbers within conserved Z-specific genes such as , , , , and , which are absent from the W chromosome. A total of 34 samples were included in this study from the following 17 bird species: domestic pigeon (), domestic chicken (), domestic goose (), domestic duck (), Mute swan (), Budgerigar (), Lovebird (), Cockatiel (), Red-rumped parrot (), Rose-ringed parakeet (), African grey parrot (), domestic Canary (), Goldfinch (), Gouldian Finch (), Red Siskin (), Australian Zebra Finch (), and Common buzzard (). The results proved the , , , , and genes can reveal the sexes in the birds tested. - Source: PubMed
Publication date: 2025/01/20
Turcu Maria-CarmenPaștiu Anamaria IoanaBel Lucia-VictoriaDoboși Anca-AlexandraPusta Dana Liana