PDGF-bb, human
- Known as:
- PDGF-bb, H. sapiens
- Catalog number:
- P716-250
- Product Quantity:
- 250 ug
- Category:
- -
- Supplier:
- 101 Bio.
- Gene target:
- PDGF- human
Related genes to: PDGF-bb, human
- Gene:
- PDGFA NIH gene
- Name:
- platelet derived growth factor subunit A
- Previous symbol:
- -
- Synonyms:
- PDGF1, PDGF-A
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- PDGFRA NIH gene
- Name:
- platelet derived growth factor receptor alpha
- Previous symbol:
- -
- Synonyms:
- CD140a, PDGFR2, GAS9
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2019-04-23
- Gene:
- PDGFRB NIH gene
- Name:
- platelet derived growth factor receptor beta
- Previous symbol:
- PDGFR
- Synonyms:
- JTK12, CD140b, PDGFR1
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: PDGF-bb, human
Related articles to: PDGF-bb, human
- Sus scrofa has been domesticated under diverse environments and management systems, leading to broad variation in genetic architecture and physiological regulation. This diversity has been preserved in indigenous breeds maintained under traditional husbandry and further expanded through modern crossbreeding programs designed to combine the distinctive attributes of native and commercial lineages. To investigate how such lineage diversity is reflected at the structural genomic level, whole-genome sequencing data from 110 pigs representing 13 populations were analysed to characterize genome-wide copy number variation (CNV) patterns and identify regions showing differential CNV patterns among lineages. Comparative analysis revealed distinct CNV landscapes between indigenous and commercial groups, encompassing 282 significantly differentiated CNV regions (CNVRs). Selection signatures defined by V and Wilcoxon tests highlighted genes involved in lipid metabolism (FAR2, MGLL, FASN), suggesting that CNV differences may underlie the characteristic fat-deposition traits of native breeds. Within the same analytical framework, crossbred populations exhibited inheritance patterns consistent with parental lineage influence: native-like CNVRs harboured lipid-associated genes (ADIPOR1, MLXIPL, GPIHBP1), whereas commercial-like CNVRs contained loci related to muscle development and growth (CAPN1, PDGFA, EEF1A2, SH2B1). These results collectively provide genomic insight into how CNVs reflect the effects of historical adaptation and selective breeding in domestic pigs. The differentiated CNVRs identified here encompass genes involved in fat deposition and muscle biology, suggesting potential links to trait variation across lineages. This work offers a genomic foundation for future studies integrating CNV and functional traits, and highlights the value of structural variation in informing crossbreeding and breed-improvement strategies. - Source: PubMed
Kim BongsangSeo JeongwooKim HeebalKim Young-SinLee JonganCho Seoae - Hepatocellular carcinoma (HCC) typically develops from liver cirrhosis (LC), however early diagnosis is difficult due to a lack of reliable biomarkers. The goal of this study was to use SomaScan proteomics technology to find plasma protein profiles that differentiated LC and HCC from healthy controls in order to develop novel biomarkers for HCC early detection and targeted therapy. - Source: PubMed
Publication date: 2026/06/01
Huang LingyuGuo JunjunLiu WeiXie ShenpingYan QiangPu WenjunZeng ZhipengLai LiushengWang BaoyaoDai YongTang DongeChen Huaizhou - Tendon injuries pose significant clinical challenges because tendon tissue has limited intrinsic healing capacity, often resulting in poor functional recovery. In exploring novel therapeutic strategies, we found that Mucin 1 (Muc1), a key regulator of tissue repair, is transiently upregulated during the early stages of tendon injury. We therefore hypothesized that sustained activation of this naturally transient signal would promote tendon repair. To validate this hypothesis, we developed a nanoparticle-based gene delivery system to achieve sustained Muc1 expression in a rat model of tendon injury. This targeted intervention significantly improved tendon healing, primarily by creating a pro-regenerative microenvironment. Mechanistically, we demonstrated that Muc1 activation stimulates endothelial cells to secrete platelet-derived growth factor A (PDGFA), which promotes tendon cell proliferation, particularly when packaged within extracellular vesicles. Collectively, those findings support Muc1 as a potent therapeutic target. The nanoparticle-mediated Muc1 gene delivery strategy offers a highly promising regenerative approach for tendon injury treatment with direct translational potential. - Source: PubMed
Publication date: 2026/04/30
Xue YanSun JieJi Xu HaoWang RongShi Jia YuYang Qian QianZhou You LangTan Jun - The prevalence of diabetes mellitus (DM) is increasing daily worldwide. DM patients suffer from numerous complications, including the development of chronic wounds that can lead to amputation. These complications necessitate innovative approaches. As part of these innovative approaches, this study synthesized four chalcone derivatives and evaluated their activities in an in vitro diabetic wound model. Several spectroscopic techniques, including 1 H and 13 C NMR and HR-MS, were used to confirm the structures of the newly synthesized compounds. After investigating the inhibition of α-glucosidase in HDF-1 cells treated with D-glucose (50 mM), MTT tests and scratch tests were performed. Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), total antioxidant status (TAS), and procollagen type-1 were analyzed using an ELISA kit. Additionally, proliferation (Ki67), inflammatory (Nuclear factor kappa B; NFκB), and growth factor (Platelet-derived growth factor subunit A; PDGFA) markers in fibroblasts were assessed by immunohistochemistry. All compounds exhibited strong α-glucosidase inhibitory activity, with IC₅₀ values ranging from 1.115 to 1.612 µg/mL. Cytotoxicity analysis demonstrated that all compounds were biocompatible, maintaining over 85% cell viability in HDF-1 cells. Under diabetic conditions, treatment significantly improved cell viability and promoted wound closure, particularly in C4. In addition, the compounds reduced pro-inflammatory cytokines TNF-α and IL-1β while increasing TAS and procollagen type I levels. Immunocytochemical findings revealed enhanced Ki67 and PDGFA expression and decreased NFκB activation in treated groups. Molecular docking analysis supported the experimental findings by demonstrating favorable binding interactions with α-glucosidase. In conclusion, chalcone derivatives-particularly compound C4-promote diabetic wound healing through multitarget mechanisms involving anti-inflammatory, antioxidant, and pro-regenerative effects, highlighting their strong therapeutic potential. - Source: PubMed
Publication date: 2026/05/08
Demirbağ BurcuÜnver HakanKara AyçaNecip AdemYıldırım Metin - Cellular senescence is a multifaceted stress response marked by stable proliferative arrest and the secretion of diverse biologically active factors, collectively known as the senescence-associated secretory phenotype (SASP). The senescent phenotype is remarkably variable and subject to various regulatory influences. We previously demonstrated that mitochondrial dysfunction induced by diverse stimuli, including the loss of sirtuin 3 (SIRT3), leads to the hyperactivation of AMPK and p53, culminating in senescence while concurrently suppressing much of the proinflammatory SASP. Here, we extend our findings by revealing that the absence of SIRT3 can suppress segments of the SASP even in the absence of p53. Intriguingly, SIRT3 deficiency renders cells resistant to stimulation by exogenous cytokines, such as interleukin-1. Fibroblasts derived from Sirt3 knockout mice exhibit a diminished SASP, including reduced levels of Pdgfa, and these mice display impaired wound healing and a more expansive granulation area. Furthermore, aged Sirt3 knockout mice show disrupted patterns of senescence relative to wild type controls, including increases in senescence markers in adipose tissue, but surprisingly also decreases in liver and heart. Collectively, these data underscore a role for SIRT3 in orchestrating cellular senescence phenotypes, shedding light on its regulatory influence beyond the p53-dependent pathway. - Source: PubMed
Publication date: 2026/05/06
Kura NiharikaMogck Bronwyn AJezak Samantha TVelarde Michael CWiley Christopher D