Nkx6.1 (delta C)

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797.36 €

Known as:: Nkx6.1 (delta C)
Catalog number:: 000717A
Product Quantity:: 250ul
Category:: -
Supplier:: ABM
Gene target:: Nkx6.1 (delta )

Related genes to: Nkx6.1 (delta C)

Gene:: AGPAT4 ^{NIH gene}
Name:: 1-acylglycerol-3-phosphate O-acyltransferase 4
Previous symbol:: -
Synonyms:: LPAAT-delta, dJ473J16.2
Chromosome:: 6q26
Locus Type:: gene with protein product
Date approved:: 2003-11-25
Date modifiied:: 2019-03-26

Gene:: CEBPD ^{NIH gene}
Name:: CCAAT enhancer binding protein delta
Previous symbol:: -
Synonyms:: CRP3, CELF, C/EBP-delta, NF-IL6-beta
Chromosome:: 8q11.21
Locus Type:: gene with protein product
Date approved:: 1992-06-24
Date modifiied:: 2018-02-23

Gene:: CSNK1D ^{NIH gene}
Name:: casein kinase 1 delta
Previous symbol:: -
Synonyms:: HCKID, CKID, CKIdelta
Chromosome:: 17q25.3
Locus Type:: gene with protein product
Date approved:: 1995-09-27
Date modifiied:: 2016-10-05

Gene:: DGKD ^{NIH gene}
Name:: diacylglycerol kinase delta
Previous symbol:: -
Synonyms:: KIAA0145, DGKdelta
Chromosome:: 2q37.1
Locus Type:: gene with protein product
Date approved:: 1998-10-02
Date modifiied:: 2016-10-05

Gene:: EIF2B4 ^{NIH gene}
Name:: eukaryotic translation initiation factor 2B subunit delta
Previous symbol:: -
Synonyms:: EIF2Bdelta, EIF-2B, DKFZP586J0119, EIF2B
Chromosome:: 2p23.3
Locus Type:: gene with protein product
Date approved:: 1998-10-16
Date modifiied:: 2015-11-16

Related products to: Nkx6.1 (delta C)

Related articles to: Nkx6.1 (delta C)

Physical and Biochemical Determinants of Endocrine Fate in 3D Suspension Culture Based Stem Cell-Derived β-Cell Differentiation.
Efficient and reproducible generation of functional stem cell-derived β cells (sBC) remains a major challenge for basic research and cell replacement therapy, partly due to incomplete understanding of endocrine induction during differentiation and challenges with clinical scale-up. Here, we dissect the individual contributions of commonly used endocrine differentiation factors on pancreatic progenitor maintenance, endocrine commitment, and hormone subset generation in a scalable 3D differentiation system. We demonstrated that starting pluripotent stem cell cluster size is a critical determinant for downstream sBC generation. We also verify that a commonly employed combination of endocrine induction molecules efficiently drives endocrine lineage commitment but yields limited β-cell generation. Detailed analysis of the effects of individual endocrine induction molecules revealed distinct effects: EGF or KGF preserved NKX6.1 progenitors without induction of endocrine differentiation; Notch or BMP inhibition robustly induced endocrine marker expression but concurrently reduced NKX6.1 expression, resulting in predominant generation of glucagon-expressing cells; retinoic acid, thyroid hormone (T3), or TGFβ inhibition maintained high NKX6.1 levels while also promoting efficient insulin endocrine differentiation. These findings indicate NKX6.1 protein maintenance as a key determinant of human β-cell generation and show that endocrine differentiation factors exert divergent effects on lineage progression. - Source: PubMed
Publication date: 2026/09/02
Castro-Gutierrez RobertoShilleh Ali HBarra Jessie MWilliams Shane P MNedumaran BalachandarTriolo Taylor MHebrok MatthiasRuss Holger A
Esculetin induces apoptosis and functional impairment in INS-1 pancreatic β-cells associated with ER stress and MAPK/JNK signaling.
Esculetin, a coumarin derivative, exhibits diverse biological activities; however, its impact on pancreatic β-cell stress responses and survival remains poorly defined. In this study, we investigated the effects of esculetin on cellular stress signaling, apoptosis, and functional gene expression in INS-1 pancreatic β-cells. Following treatment with 3000 µM esculetin for 6 h, cell viability, proliferation, apoptosis, oxidative stress, endoplasmic reticulum (ER) stress markers, MAPK signaling components, cell cycle distribution, and β-cell-specific gene expression were assessed. In silico molecular docking was performed to explore putative interactions between esculetin and proteins involved in ER stress, MAPK signaling, and apoptosis. Treatment with 3000 µM esculetin for 6 h increased apoptotic cell death by approximately 32-fold and elevated total oxidation status and oxidative stress index. Intracellular insulin, Ca²⁺, and CA19-9 levels were increased, accompanied by cell cycle arrest characterized by G0/G1 phase accumulation and a reduction in the G2/M population. Expression of ER stress sensors ATF6, IRE1α, and CHOP was upregulated, whereas PERK expression was reduced. In parallel, MAPK/JNK pathway activation was evidenced by increased levels of p-ATF2, p-c-Jun, and HSP90, along with decreased p-Elk1. Gene expression analysis revealed marked downregulation of β-cell functional and identity-associated genes, including Ins1, Ins2, IR, Akt, MafA, Nkx6.1, Pdx1, NeuroD1, and Pax6, while FoxO1 expression was upregulated. Collectively, these findings suggest the involvement of ER stress-associated MAPK/JNK signaling in esculetin-induced apoptosis and functional impairment in INS-1 pancreatic β-cells, providing mechanistic insight into stress-associated β-cell dysfunction. - Source: PubMed
Publication date: 2026/08/29
Karatug Kacar Ayse
MAFB in Pancreatic β-Cell Development and Dysfunction: Implications for Diabetes and Translational Applications.
Large MAF transcription factors, including MafA and MafB, are essential for maintaining β-cell identity, function and survival. While MafA has been widely studied in pancreas development and type 2 diabetes, the extended roles of MafB in humans are still emerging. During embryogenesis, MafB promotes differentiation of β-cells. While MafB is downregulated in adult mouse β-cells, it remains active in adult human β-cells, indicating important species-specific functions. Mechanistically, MafB cooperates with other β-cell-specific transcription factors, including PDX1, NEUROD1 and NKX6.1, to regulate genes critical for β-cell differentiation and insulin expression. Loss of MafB in human β-cells is associated with hallmark features of diabetic pathology, such as dedifferentiation, impaired insulin production, and transdifferentiation under metabolic stress. In addition to its endocrine roles within islets, MafB regulates macrophage polarization and apoptotic cell clearance, suggesting immune-metabolic interactions that may contribute to islet inflammation and dysfunction. Translationally, MafB may be leveraged to enhance stem-cell-derived β-cell differentiation and maturation and support β-cell identity preservation under stress and potentially immune responses; however, these applications remain to be further studied and validated. In this review, we integrate findings from developmental biology, animal models, and human studies to clarify the overarching role of MafB in bridging β-cell development, immune regulation, and potential translational application in stem-cell therapy or as a biomarker target in diabetes research. - Source: PubMed
Publication date: 2026/07/23
Mu-U-Min Razik Bin AbdulDiane AbdoulayeAl-Siddiqi Heba Hussain
Polystyrene Nanoplastics Drive β-Cell Dedifferentiation Through Dendritic Cell-Intrinsic MHC-I-Dependent Inflammatory Crosstalk.
Environmental nanoplastic exposure is linked to metabolic disorders, yet its impact on pancreatic immune-endocrine homeostasis and β-cell identity regulation remains poorly defined. Rats were exposed to polystyrene nanoplastics(PS-NPs) for 12 weeks under a control or high-fat diet. Pancreatic injury and phenotypes were assessed biochemically, histologically, and ultrastructurally; single-nucleus RNA-seq delineated cell-specific transcription and intercellular networks. Mechanistic validation used cell co-cultures with MHC-I modulation, and translational relevance was assessed in a human exposure cohort. Chronic PS-NPs exposure exacerbated hyperglycemia and glucose intolerance, and induced pancreatic damage. Single-nucleus transcriptomics identified β cells and dendritic cells (DCs) as the most responsive populations. PS-NPs drove β-cell dedifferentiation, characterized by downregulation of key identity markers (Mafa, Pdx1, Nkx6.1). Concurrently, DCs exhibited a maturation-like phenotype with robust upregulation of MHC-I and inflammatory pathways. Ligand-receptor analysis revealed enhanced proinflammatory crosstalk between DCs and β cells. Functionally, MHC-I upregulation in DCs activated TLR4/NF-κB signaling and drove β-cell dedifferentiation in vitro. Consistently, occupationally exposed individuals showed elevated circulating HLA-A levels and metabolic abnormalities. These findings identify an MHC-I-dependent DCs-β-cell inflammatory axis through which PS-NPs disrupt pancreatic immune-endocrine homeostasis and promote β-cell dedifferentiation, revealing mechanisms underlying PS-NPs-induced metabolic dysfunction. - Source: PubMed
Publication date: 2026/08/17
Qiao ConghuiSong YuqingYang FangGuo MenghuiJiang LibinQuan XiaoyueWei WeiWang XinyangHan TianshuLiu MingyuanJiang Wenbo
Pluripotency-Preserving Culture System for Pancreatic Stellate Cells Using MSC Medium: From Quiescence Maintenance to Regenerative Potential.
Pancreatic stellate cells (PSCs) play a central role in pancreatic physiology and disease, and the transition between their quiescent and activated states influences processes such as fibrosis and regeneration. However, the stem cell-like properties of PSCs remain unclear. This study aims to clarify the stem cell characteristics of PSCs and establish a method to maintain their quiescent state, thereby providing a new perspective on pancreatic regeneration. - Source: PubMed
Publication date: 2026/07/30
Cai ZhenShengNi ChengmingWang QianQianWang XiaohangWang HuanChen YangGuo YanLin HaoSun BoQiu ShanhuSun Zilin

Nkx6.1 (delta C)

Related genes to: Nkx6.1 (delta C)

Related products to: Nkx6.1 (delta C)

Related articles to: Nkx6.1 (delta C)

Physical and Biochemical Determinants of Endocrine Fate in 3D Suspension Culture Based Stem Cell-Derived β-Cell Differentiation.

Esculetin induces apoptosis and functional impairment in INS-1 pancreatic β-cells associated with ER stress and MAPK/JNK signaling.

MAFB in Pancreatic β-Cell Development and Dysfunction: Implications for Diabetes and Translational Applications.

Polystyrene Nanoplastics Drive β-Cell Dedifferentiation Through Dendritic Cell-Intrinsic MHC-I-Dependent Inflammatory Crosstalk.

Pluripotency-Preserving Culture System for Pancreatic Stellate Cells Using MSC Medium: From Quiescence Maintenance to Regenerative Potential.