anti ccnd1  (Cell Signaling Technology Inc)

Journal: International Journal of Molecular Medicine

Article Title: m 6 A in adipose tissue inflammation: A novel regulator of obesity and metabolic diseases (Review)

doi: 10.3892/ijmm.2026.5795

Figure Lengend Snippet: Role of m 6 A in adipogenesis. Insufficient adipogenesis in adipose tissue leads to persistent, chronic inflammation. m 6 A modification plays a crucial role in all stages of adipogenesis, from commitment to terminal differentiation. During commitment, METTL3 promotes lipogenic differentiation in BMSCs by regulating the m 6 A levels of PTH1R and JAK1, whereas silencing METTL14 reduces the expression of SMAD1, inhibiting BMSC proliferation. During terminal differentiation, m 6 A regulates MCE and the transition to mature adipocytes. FTO influences key genes such as ATG5, ATG7 and JAK2, affecting autophagy, STAT3 phosphorylation and adipogenesis. FTO knockout increases the m 6 A levels of CCND1 and CDK2, blocking MCE. m 6 A, N6-methyladenine; METTL, methyltransferase-like; PTH1R, parathyroid hormone 1 receptor; JAK, Janus kinase; BMSC, bone marrow mesenchymal stem cell; MCE, mitotic clone amplification; FTO, Fat mass and obesity-associated protein; ATG, autophagy-related; STAT3, signal transducer and activator of transcription 3; CCND1, cyclin D1; CDK2, cyclin-dependent kinase 2; IGF2BP1, insulin-like growth factor 2 mRNA-binding protein 1; YTHDF2, YTH domain family 2.

Article Snippet: In addition, for mitotic clone amplification (MCE) in the early stage of terminal differentiation, the inhibition of FTO expression in 3T3-L1 cells leads to increased m 6 A methylation levels of cyclin D1 (CCND1) and cyclin-dependent kinase 2, the protein expression of which is reduced after recognition by YTHDF2, resulting in blockade of the MCE process and in turn the inhibition of lipogenesis ( ) ( ).

Techniques: Modification, Expressing, Phospho-proteomics, Knock-Out, Blocking Assay, Amplification, Binding Assay

Journal: International Journal of Molecular Medicine

Article Title: m 6 A in adipose tissue inflammation: A novel regulator of obesity and metabolic diseases (Review)

doi: 10.3892/ijmm.2026.5795

Figure Lengend Snippet: Role of m 6 A in ATMs. ATMs are deeply involved in adipose tissue inflammation, and m 6 A plays critical roles in macrophage biology, including their development, activation, pyroptosis and metabolism of lipids. (A) m 6 A regulates macrophage development by targeting genes such as CCND1 and ATRX via YTHDF3, ALKBH5 and METTL3, affecting haematopoietic stem and progenitor cell differentiation. (B) m 6 A modification mediated by METTL3, METTL14 and IGF2BP2 controls macrophage activation and polarization by influencing key genes such as SPRED2, MYD88 and STAT1, which impact the NF-κB and PPAR-γ pathways. (C) m 6 A regulates macrophage pyroptosis by targeting CASPASE-1, IL-1β and MALAT1 and modulating pathways such as the PTBP1/USP8/TAK1 pathway. (D) Additionally, m 6 A affects macrophage lipid metabolism by regulating lipid uptake and cholesterol efflux through MSR1 and SR-B1. m 6 A, N6-methyladenine; ATMs, adipose tissue macrophages; CCND1, cyclin D1; ATRX, α-thalassemia X-linked intellectual disability syndrome; YTHDF3, YTH domain family 3; ALKBH5, alkB homologue 5; METTL, methyltransferase-like; IGF2BP2, insulin-like growth factor 2 mRNA-binding protein 2; SPRED2, sprouty-related EVH1 domain-2; MYD88, myeloid differentiation primary response 88; STAT1, signal transducer and activator of transcription 1; NF-κB, nuclear factor-κB; PPAR-γ, peroxisome proliferator-activated receptor γ; CASPASE-1, cysteinyl aspartate specific proteinase-1; IL, interleukin; MALAT1, metastasis-associated lung adenocarcinoma transcript 1; PTBP1, polypyrimidine tract-binding protein 1; USP8, ubiquitin-specific peptidase 8; TAK1, TGFβ-activated kinase 1; MSR1, macrophage scavenger receptor 1; SR-B1, scavenger receptor type B1; ROS, reactive oxygen species; TSC1, tuberous sclerosis complex 1; SOCS2, suppressor of cytokine signalling 2; GSDMD-N, gasdermin D N-terminal domain; OxLDL, oxidized low-density lipoprotein; MSR1, macrophage scavenger receptor 1; DDX5, DEAD-box helicase 5; MEHP, mono(2-ethylhexyl) phthalate.

Article Snippet: In addition, for mitotic clone amplification (MCE) in the early stage of terminal differentiation, the inhibition of FTO expression in 3T3-L1 cells leads to increased m 6 A methylation levels of cyclin D1 (CCND1) and cyclin-dependent kinase 2, the protein expression of which is reduced after recognition by YTHDF2, resulting in blockade of the MCE process and in turn the inhibition of lipogenesis ( ) ( ).

Techniques: Activation Assay, Cell Differentiation, Modification, Binding Assay, Ubiquitin Proteomics

Journal: International Journal of Molecular Medicine

Article Title: Astragaloside IV targets TUBB4B to inhibit proliferation and promote apoptosis of pituitary tumor cells via the STMN1/ERK pathway

doi: 10.3892/ijmm.2026.5822

Figure Lengend Snippet: OE-TUBB4B upregulates STMN1 and activates the ERK pathway. (A) Effect of TUBB4B on GH3 cell cycle progression. (B) Cell cycle distribution. (C) Reverse transcription-quantitative PCR was used to assess the effects of OE-TUBB4B. (D) Transcriptomic sequencing showing Kyoto Encyclopedia of Genes and Genomes pathway enrichment of differentially expressed genes. (E) Transcriptomic sequencing showing the protein-protein interaction network of proteins that interact with TUBB4B (red box indicates key pathway proteins that interact with TUBB4B). (F) Interaction diagram between the TUBB4B and STMN1 proteins from STRING. (G) Cell Counting Kit-8 assay was used to assess the viability of GH3 cells treated with U0126. In GH3 cell lines treated with U0126, the protein expression levels of (H) STMN1, (I) p-STMN1 (I), and cPLA2 (J) were assessed by western blotting (K), and levels of p-cPLA2 (L), ERK (M), p-ERK (N), CCND1 (O), JNK (P), and p-JNK (Q) were also assessed. **** P<0.0001, *** P<0.001, ** P<0.01, * P<0.05 vs. vector. OE, overexpression; TUBB4B, tubulin beta 4B class IVb; STMN1, stathmin 1; p-, phosphorylated; cPLA2, cytosolic phospholipase A2; CCND1, cyclin D1; KD, knockdown; OD, optical density; ns, not significant.

Article Snippet: CCND1 antibody , Boster Biological Technology , PB0403.

Techniques: Reverse Transcription, Real-time Polymerase Chain Reaction, Sequencing, Cell Counting, Expressing, Western Blot, Plasmid Preparation, Over Expression, Knockdown

Journal: Cell Genomics

Article Title: Hi-C for genome-wide detection of enhancer-hijacking rearrangements in routine lymphoid cancer biopsies

doi: 10.1016/j.xgen.2026.101166

Figure Lengend Snippet: Structural variants detected by FFPE Hi-C in lymphoid biopsies (A) Overview of SV detection across the cohort. Comparison of detection by Hi-C versus clinical cytogenetics/FISH is shown at the right for selected rearrangements. Samples are ordered and colored as in A. (B) Schematic diagram of SV detection by Hi-C. (C and D) Balanced Hi-C matrices showing gene fusions ETV6::RUNX1 (C) and NPM1::ALK (D) in the indicated biopsies. (E) Top: balanced Hi-C matrix for DLBCL biopsy DL11 showing a reconstructed IGH::BCL2 rearrangement. Blue circle indicates a significant neo-loop (NeoLoopFinder) between an IGH 3′RR enhancer and the BCL2 promoter. Bottom: virtual 4C tracks ( BCL2 promoter viewpoint) from eight DLBCL samples with IGH::BCL2 rearrangements. (F) Top: balanced Hi-C matrix for PCN biopsy PL12 showing a reconstructed IGH::CCND1 rearrangement. Blue circles indicate significant neo-loops (NeoLoopFinder) between IGH 3′RR enhancers and the CCND1 promoter. Bottom: virtual 4C tracks ( CCND1 promoter viewpoint) for eight PCN and MCL samples with IGH::CCND1 rearrangements. (G) Left: balanced Hi-C matrix showing IGL::BCL2 rearrangement in biopsy DL03. Blue circles indicate significant neo-loops (NeoLoopFinder) to the BCL2 promoter region. Right: immunohistochemistry showing aberrant co-expression of BCL2 with GCB markers CD10 and BCL6 in DL03. (H and I) Balanced Hi-C matrices showing putative enhancer-hijacking rearrangements IGH::CCND2 (H) and IGH::MAFB (I) in the indicated biopsies. Blue circles indicate significant neo-loops (NeoLoopFinder) to the promoter of the displayed gene, while the black arrow indicates other regions of apparently increased Hi-C interactions between enhancers and oncogene promoters.

Article Snippet: Vysis IGH/CCND1 DF FISH Probe Kit , Abbott Laboratories , 08L58-020 00884999031487.

Techniques: Hi-C, Comparison, Immunohistochemistry, Expressing