PDGFD antibody
- Known as:
- PDGFD (anti-)
- Catalog number:
- orb101253
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- PDGFD antibody
Related genes to: PDGFD antibody
- Gene:
- PDGFD NIH gene
- Name:
- platelet derived growth factor D
- Previous symbol:
- -
- Synonyms:
- SCDGF-B, MSTP036, IEGF
- Chromosome:
- 11q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-22
- Date modifiied:
- 2015-08-25
Related products to: PDGFD antibody
Related articles to: PDGFD antibody
- Malocclusion is a common oral health problem with a strong hereditary component. Previous genetic studies were limited by small sample sizes and low genomic coverage. To address these limitations, we conducted a genome-wide association study (GWAS) using array-based genotype data in 5 large, multiancestral cohorts. The study included 3,405 participants from the United States and its territories, the Philippines, Colombia, and Nigeria. Class II malocclusion was defined as an Angle's class II molar relationship with an overjet >3.5 mm, class III malocclusion as an Angle's class III molar relationship with a negative overjet, and class I malocclusion (controls) as an Angle's class I molar relationship with an overjet of 0 to 3.5 mm. In the vertical plane, an anterior open bite of any magnitude was classified as "open bite," while an overbite >3.5 mm was classified as "deep bite," with controls having an overbite of 0 to 3.5 mm. Multiplanar malocclusion included cases with both sagittal and vertical discrepancies, with controls having an Angle's class I molar relationship, an overjet of 0 to 3.5 mm, and an overbite of 0 to 3.5 mm. GWAS for each phenotype was conducted within individual cohorts before meta-analysis. We identified genome-wide significant associations ( ≤ 5E-08) at 11q22.3 (rs372564249, odds ratio [OR] = 3.12) and 3p24.3 (rs13060317, OR = 2.4) for class II and multiplanar malocclusion, respectively. Additionally, we observed a near-significant signal at 12q15 (rs1261646, OR = 1.9, = 6.2 × 10) for class II malocclusion and a suggestive association at 1p21.3 (rs7541224, OR = 2.0, = 1.7 × 10) for class III malocclusion. The 11q22.3 and 3p24.3 loci were QTLs for the and genes, and transcriptomic data showed consistent expression of these genes during facial development. These findings provide valuable insights into malocclusion etiology and lay the groundwork for genetic risk score development. - Source: PubMed
Publication date: 2026/06/15
Alade AMaurer J MAnderton JLee M-KAlmpani KGoovaerts SClaes PButali AAdeyemo ALevy SHartsfield J KMorford L APeter TMiller SMcNeil D WShaffer J RFoxman BWeinberg S MMoreno Uribe L MMarazita M LLee J S - Excessive fat accumulation in the sheep tail is no longer aligned with modern breeding objectives. While genome-wide association studies have identified associated loci, revealing the causal variants remains challenging. To address this gap, we report an epigenetic multi-omics atlas from fat-tailed and thin-tailed sheep, focusing on functional elements, chromatin states, and their associated functions. Alterations in A/B compartments, topologically associating domains, and chromatin-specific loops were discovered. Particularly, we detected differentially expressed genes in altered compartments, modifications in contact domains, and loop formation related to adipogenesis, such as ADAMTS1, ELOVL6, BMPER, PDGFD, and VEGFA. Among these genes, we confirmed a novel enhancer-promoter loop at the ADAMTS1 locus in fat-tailed sheep. Disruption of this regulatory element reduces ADAMTS1 expression, thereby promoting adipogenesis in preadipocytes. In addition, a downstream copy number deletion (chr20: 17301600-17,302,600) near VEGFA in conjunction with an enhancer region (chr20:17302162-17,302,561). Functional validation using CRISPR/Cas9-mediated knockout of this enhancer significantly suppressed VEGFA expression, whereas dCas9-P300-mediated activation enhanced its transcriptional activity. Furthermore, transcription factor KLF15 binds to the promoter and enhancer regions of VEGFA, thereby promoting preadipocyte differentiation. During this critical process, KLF15 facilitated interaction between its direct transcriptional targets and the coactivator P300, thereby recruiting P300 to the promoter region. Our findings emphasize multiscale 3D epigenome reprogramming during fat tail formation and unveil intricate transcriptional control mechanisms, encompassing cooperative regulation by enhancers, transcription factors, and co-activator factors. This study presents novel insights into the intrinsic molecular mechanisms of the "Enhancer-TFs-Promoter" complex, which underlies adipogenesis, the fat tail trait, and obesity-related human diseases. - Source: PubMed
Publication date: 2026/06/11
Jin MeilinQuan KaiWang HaoWang HuihuaDu LixinLi TaotaoChu MingxingSun DongxiaoWei Caihong - Vascular calcification (VC), characterized by calcium deposition in arterial walls, is a major risk factor for cardiovascular morbidity and mortality. While genome-wide association studies (GWAS) have identified susceptibility loci for specific vascular beds, such as coronary artery calcification (CAC) and abdominal aortic calcification (AAC), single-phenotype studies may overlook pleiotropic variants. This study aims to elucidate the shared genetic architecture of CAC and AAC and translate these findings into biological insights and potential therapeutic targets. - Source: PubMed
Publication date: 2026/05/15
Li HuibinLi Gaofei - PURPOSE: Adrenal myelolipoma (AML) is a benign tumor composed of intermixed adipose and hematopoietic tissues, but its detailed cellular composition remains unclear. CXCL12-abundant reticular (CAR) cells have been found to promote hematopoiesis during AML development; however, the mechanism of adipogenesis in AML remains unclear. This study aimed to characterize the cellular composition of AML and elucidate the potential mechanisms underlying its development, with a particular focus on adipocyte origin. METHODS: Four AML specimens and matched adjacent adrenal tissues were subjected to single-nucleus RNA sequencing, and an additional ten paired samples were analyzed using immunostaining. Complementary in vitro experiments were performed to validate the proposed mechanisms of AML development. RESULTS: Unsupervised clustering revealed that AML is composed predominantly of T cells, B cells, neural-like cells, CAR cells, adipocytes, and nearly all types of myeloid cells. RNA velocity analysis suggested that CAR cells might be the lineage source of adipocytes. Consistently, CAR cells isolated from AML tissues demonstrated adipogenic capacity in vitro. Expression analysis showed high levels of adrenocorticotropic hormone receptor and androgen receptor in adrenal cortical cells and endothelial cells respectively. CellChat analysis further revealed extensive paracrine signals from adrenal cortical cells and endothelial cells to CAR cells. Overexpression of androgen receptor in endothelial cells transcriptionally upregulated key regulators of adipogenesis including COL4A1 and PDGFD. CONCLUSIONS: AML comprises a heterogeneous population of immune and stromal cells, with CAR cells likely serving as the primary source of adipocytes. Moreover, androgen may regulate CAR cells to induce adipocytes via endothelial cells. - Source: PubMed
Publication date: 2026/05/02
Guo GuodongGuo ZhonghaoSong WenbinWang KeYe LeihongLi BuyunZhang LinlinLiu TaoLi XudongLi LeiChen Yule - The role of platelet-derived growth factor D () in mesenchymal cells is well-established, but its specific function in skeletal muscle generation remains unknown. This study reveals for the first time PDGFD's dual regulatory role in myogenesis: it acts both as a "guardian" maintaining the myoblast pool and as an "initiator" driving myogenic differentiation. Through single-cell RNA sequencing analysis of skeletal muscle from , we identified as a common candidate gene for both muscle and fat development. In the C2C12 cell model, knockdown significantly inhibited cell proliferation and promoted apoptosis, while overexpression enhanced viability and inhibited apoptosis, indicating its critical role in maintaining myoprogenic precursor cell homeostasis. Further studies revealed that interference downregulated key myogenic differentiation markers and , inhibiting differentiation. Its expression peaked during mid-differentiation (D5), suggesting temporal regulation of differentiation. Interestingly, although primarily acts through the PI3K/Akt pathway downstream of , knockdown did not show significant synergistic effects with PI3K/Akt pathway activation in inhibiting differentiation. This suggests may specifically regulate myogenic differentiation via an independent or parallel signaling axis. This study not only expands the known functions of in muscle biology but also provides new insights into the mechanisms by which growth factors coordinate cell fate decisions. - Source: PubMed
Publication date: 2026/03/18
Cao HongzhenWang JingWang YunzhouHuang JingsenChen WeiTang HuiChen JunfengXing BaosongZeng Yongqing