NeuroD1
- Known as:
- NeuroD1
- Catalog number:
- 000450A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- NeuroD1
Related genes to: NeuroD1
- Gene:
- NEUROD1 NIH gene
- Name:
- neuronal differentiation 1
- Previous symbol:
- NEUROD
- Synonyms:
- BETA2, BHF-1, NeuroD, bHLHa3, MODY6
- Chromosome:
- 2q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-12
- Date modifiied:
- 2019-04-23
Related products to: NeuroD1
Related articles to: NeuroD1
- Small cell lung cancer (SCLC) is a highly aggressive malignancy with limited therapeutic options. Immune checkpoint inhibitors (ICIs) modestly improve outcomes, but predictive biomarkers are lacking. CD73, an ecto-5'-nucleotidase, generates immunosuppressive adenosine and may attenuate ICI efficacy. - Source: PubMed
Publication date: 2026/04/25
Saiki MasafumiInoue TomohiroTakusagawa KazuhoHomma KentaFuruya SatoshiShimamura SoOmori ChisaIde ShuichiroHoshino YukiUchida YoshinoriYamaguchi YoheiIkemura ShinnosukeKondo TetsuoSoejima Kenzo - Small-cell lung cancer (SCLC) is an aggressive neuroendocrine malignancy characterized by rapid proliferation, early metastasis, and poor prognosis. Although initially sensitive to chemotherapy and radiotherapy, most patients relapse rapidly, and long-term survival remains uncommon. Platinum-etoposide has long been the standard first-line therapy, and the recent incorporation of immune checkpoint inhibitors (ICIs) such as atezolizumab (IMpower133) and durvalumab (CASPIAN, ADRIATIC) has modestly improved survival, including a new role for durvalumab as a consolidation therapy in limited-stage SCLC. However, this benefit is restricted to a minority of patients, underscoring the need for novel therapeutic strategies. Emerging approaches include DLL3-directed bispecific T-cell engagers (BiTEs), such as tarlatamab and obrixtamig, which have shown promising efficacy in relapsed disease, and next-generation antibody-drug conjugates (ADCs) targeting DLL3, B7-H3, TROP2, and SEZ6. Additional modalities under investigation include chimeric antigen receptor (CAR) T-cell therapy and radioligand therapy (RLT), which aim to overcome the immunosuppressive tumor microenvironment and resistance to conventional treatments. Future therapeutic efforts will require biomarker-driven strategies that incorporate molecular subtyping (ASCL1, NEUROD1, POU2F3, and YAP1) and immune profiling to facilitate precise treatment selection. Combining ICIs, BiTEs, ADCs, and cellular or radioligand therapies in rational, evidence-based regimens represents a promising avenue to improve outcomes in this historically intractable disease. - Source: PubMed
Publication date: 2026/04/28
Nishii YuyaYamaguchi YohYoshida Tatsuya - MYC is amplified on extrachromosomal DNA (ecDNA) or homogeneously staining regions (HSRs) in group 3 medulloblastoma (G3-MB), conferring a poor prognosis. A better understanding of the mechanisms underlying MYC expression in ecDNA and HSRs could be leveraged to develop improved treatments for G3-MB. Using a structure-function approach, we identified and characterized an enhancer (ecMYC E1) that drives MYC activation specifically in G3-MB with MYC-amplified ecDNA or HSRs. The ecMYC E1 locus exhibited enhancer hallmarks exclusively in MYC-amplified G3-MB but not in other MYC-dependent cancer cell lines, including those with MYC amplification. Silencing of the ecMYC E1 enhancer significantly reduced MYC transcription, which was compensated by increases in ecDNA copy number. NeuroD1 and BRD4 interacted with each other and bind to ecMYC E1, looping the enhancer to the MYC promoter. Together, these findings define a mechanism that regulates amplified MYC gene expression within ecDNA or HSRs specifically in G3-MB. - Source: PubMed
Publication date: 2026/04/22
Friske Jake DCuisin FloreGuernalec PalomaMalone Hayden ANance StephanieBennett DeclanBurden Steven JChang Ti-ChengShi HaoWilliams Justin SValentine VirginiaPassaia Barbara D SJu BenshengAdetunji Modupeore OGeeleher PaulAbraham Brian JWu GangLi ChunliangRoussel Martine F - Impairment of pancreatic β-cell function is a primary etiology of type 2 diabetes mellitus (T2DM). The sulfated manno-glucuronan (GMn) was found to possess a backbone structure consisting of interspersing 1, 3-linked β-D-GlcpA residues and alternating 1, 2-linked α-D-Manp residues and 1, 4-linked β-D-GlcpA residues. Additionally, random sulfation occurs at the C6 position of the Man residues. GMn demonstrated no detectable cytotoxicity in MIN6 cells and attenuated palmitic acid (PA)-induced decreases in cell viability in a dose-dependent manner. Furthermore, GMn effectively reversed PA-impaired glucose-stimulated insulin secretion (GSIS) in a dose-dependent manner in both MIN6 cells and primary mouse islets. In vivo, GMn treatment significantly attenuated glycemic levels in high-fat diet/streptozotocin-induced type 2 diabetic mice, elevated β-cell insulin content, and decreased the proportions of α-, δ-, and pancreatic polypeptide (PP)-cells. Mechanistically, GMn significantly suppressed aldehyde dehydrogenase 1A3 (ALDH1A3)-mediated retinol metabolism and increased the expression of key β-cell identity/function markers, including PDX1, NKX6.1, MAFA, and NeuroD1, in pancreatic islets. Consistently, in vitro studies demonstrated that GMn counteracted PA-induced upregulation of ALDH1A3, while promoting the expression of the same set of β-cell transcription factors. Collectively, these findings indicate that GMn may enhance β-cell proliferation and reduces β-cell differentiation by downregulating ALDH1A3 expression. - Source: PubMed
Publication date: 2026/03/19
Zhang WenjingZhang FumingZou XiaotingWu NanHe SunyueLu LusiXu ChunyiXu WeiyingJin WeihuaZhou Jiaqiang - Although small cell lung cancer (SCLC) comprises transcription factor (TF)-defined molecular subtypes (ASCL1, NEUROD1, POU2F3), the extent to which these subtypes predict response to clinically effective therapy in patients-and whether therapy can select for subtype switching-remains unknown. The recent approval of the DLL3×CD3 bispecific T-cell engager tarlatamab represents one of the first meaningful advances in relapsed small cell lung cancer (SCLC) in decades, yet responses remain heterogeneous and resistance is inevitable. Here, we inferred SCLC gene expression from circulating chromatin in prospectively collected patient plasma (46 patients; 167 samples), enabling interrogation of response and acquired resistance to tarlatamab. Parallel development of the first immunocompetent syngeneic mouse model to study tarlatamab response and resistance enabled functional validation. Across species, findings converged on a central principle: TF subtype governs both initial response and acquired resistance. Therapeutic response was significantly associated with ASCL1-subtype tumors, whereas NEUROD1-subtype tumors exhibited inferior responses and POU2F3-subtype tumors were uniformly resistant, consistent with DLL3 being a direct ASCL1 transcriptional target and most highly expressed in ASCL1-positive tumors. Strikingly, one mode of acquired resistance revealed therapeutic selection for a NEUROD1-high state with concomitant DLL3 downregulation. Other resistant tumors exhibited enrichment of regulatory and exhausted T-cell programs, highlighting tarlatamab's dual-targeting mechanism of action. Together, these results reveal that tarlatamab exerts selective pressure against ASCL1-driven lineages, facilitating resistance through loss of an antigen intrinsically linked to that state. These findings underscore the clinical relevance of TF-defined molecular subtypes in human SCLC. More broadly, they highlight the power of integrating longitudinal plasma transcriptional profiling from patient plasma with functional mouse modeling to uncover clinical and biological mechanisms of response and resistance to cell-surface-targeted therapies. - Source: PubMed
Publication date: 2026/04/08
Vasseur DamienSaito ShinGulati Gunsagar SLee Garyoung GaryLaimon Yasmin NSimsek BerkayLerner MaddieCho HyeonseoLi YixiangWang TianchuSeo Ji-HeuiSavignano HunterJames BradyZhang ZeSemaan KarlJin ZhenjieDaoud Khatoun WassimNafeh GaelleNawfal RashadCooper Alissa JMiller KathrynSeager Maxwell DBrea Elliott JSmith EricChang JonathanPelletier MarcCosta CarlottaChoueiri Toni KSignoretti SabinaSands JacobBaca Sylvan CFreedman Matthew LOser Matthew G