PDGFB Antibody
- Known as:
- PDGFB Antibody
- Catalog number:
- 32219
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- PDGFB Antibody
Related genes to: PDGFB Antibody
- Gene:
- PDGFB NIH gene
- Name:
- platelet derived growth factor subunit B
- Previous symbol:
- SIS
- Synonyms:
- SSV
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-01-14
Related products to: PDGFB Antibody
Related articles to: PDGFB Antibody
- Dermatofibrosarcoma protuberans (DFSP) is a rare, slow-growing soft tissue sarcoma arising from dermal fibroblasts. Breast involvement is extremely rare, posing diagnostic and therapeutic challenges. We retrospectively reviewed eight cases of breast DFSP managed at our center over a 10-year period. The cohort included seven females and one male with a median age of 39.1 years. Clinical presentations were diverse: one patient had multiple areolar nodules, five presented with breast lumps including three with recurrent lumps, which is an uncommon presentation for DFSP, one had an ulceroproliferative growth with bleeding, and one presented following excision of a recurrent lump elsewhere with histopathology showing positive margins. Histological diagnosis was confirmed via core biopsy or block review. Four patients had classic DFSP, while three had fibrosarcomatous transformation. All cases of DFSP showed CD34 positivity. Wide local excision was performed in seven patients, and one underwent mastectomy. Two patients received adjuvant radiotherapy. No recurrence was observed within six months. Breast DFSP is rare and requires histopathological confirmation. Core biopsy with appropriate histologic features and CD34 immunostaining aids in diagnosis. Wide local excision remains the primary treatment approach. Radiotherapy is recommended in cases with close or positive margins, recurrence, metastatic disease, or when surgery is not feasible. Targeted therapy with Imatinib Mesylate, a tyrosine kinase inhibitor, is reserved for unresectable or metastatic lesions, provided the COL1A1::PDGFB translocation involving chromosomes 17 and 22 [t (17; 22)] is confirmed. Long term stringent follow up is required as recurrence in breast has been noted 26 years following primary treatment in literature. - Source: PubMed
Publication date: 2026/01/07
Surendra ShreyaSahu ShaliniRaj SanthoshDaniel NirmalSen SupriyaSam Thomas ShawnAbera MeskeremBalakrishnan RajeshCherian Anish JacobPaul Mazhunvanchary Jacob - In recent years, rare fibrosarcoma-like tumors have been identified in the gynecologic tract characterized by variable CD34 and S-100 positivity and recurrent tyrosine kinase gene fusions in many cases. We identified 17 of these tumors by searching for gynecologic sarcomas expressing S-100 and/or CD34 and supplementing these with cases contributed by collaborating institutions. Tumors involved the uterine cervix (n=11), uterine corpus (n=4), and vagina (n=2). Patients ranged from 28 to 64 (median: 50) years. Fifteen tumors showed overlapping morphologic features including haphazard or fascicular growth of relatively monotonous spindled to ovoid cells with minimal to moderate cytoplasm. Tyrosine kinase gene fusions were identified in 9 tumors, including NTRK fusions in 6 and COL1A1::PDGFB in 3 tumors. Oncogenic variants in ERBB2/ERBB3 were identified in 6 additional tumors. These two subgroups showed distinct immunohistochemical profiles, with all tyrosine kinase fusion-positive tumors being CD34 positive, variably S-100 positive, and SOX10 negative. In contrast, the ERBB-altered tumors were CD34 negative and diffusely positive for S-100 and SOX10. The remaining 2 tumors showed morphologic and immunohistochemical overlap with the tyrosine kinase fusion-positive sarcomas; one was negative for fusion or sequence variants, and sequencing failed in the other. In conclusion, most fibrosarcoma-like tumors of the gynecologic tract are defined by either tyrosine kinase fusions or ERBB2/3 mutations. Immunohistochemistry can be used to predict these subgroups to guide confirmatory genetic testing and targeted therapies. - Source: PubMed
Publication date: 2026/08/27
Marshall Emily HathewayHung Yin PQuick Charles MKatsakhyan LevonMassoth Lucas RBui Marilyn MFisch Adam SLin Lawrence HsuTurashvili GulisaOliva EstherVan de Vijver KoenCroce SabrinaBuza NataliaNielsen G PeturDevins Kyle M - Aortic dissection (AD) is a severe vascular condition marked by abrupt onset, rapid progression, and heightened mortality rates. Vascular smooth muscle cells (VSMCs), the predominant cellular component of the arterial media, are essential for maintaining the structural integrity and functionality of blood vessels. Recent studies have associated Cysteine-rich protein 2 (CSRP2) with the advancement of several vascular diseases. The involvement of CSRP2 in AD progression is unclear. Aortic tissues were collected from patients for RNA sequencing and histological analysis. A mouse model of AD was created using β-aminopropionitrile monofumarate (BAPN), while VSMC phenotypic switching was induced by platelet-derived growth factor BB (PDGF-BB). Adeno-associated virus vector was used to overexpress CSRP2 in aorta. A variety of histopathological assays and biochemical analyses were applied to determine gene and protein expression patterns as well as uncover underlying molecular mechanisms. CSRP2 was significantly downregulated in both human and murine AD, and CSRP2 gene overexpression dramatically reduced BAPN-induced AD incidence and prevented animal mortality. CSRP2 could preserve a contractile VSMC phenotype, even though under PDGF-BB stimulation. Mechanistically, our findings reveal that CSRP2 directly interacts with p130 Crk-associated substrate (p130Cas; also known as BCAR1) and reduces its phosphorylation, which in turn inhibits the activation of extracellular signal-regulated kinase (ERK) signaling pathways, thereby preventing VSMC phenotypic switching induced by PDGF-BB. Our findings identify CSRP2 as a novel regulator of VSMC phenotypic modulation and a significant modulator of AD development, suggesting its potential as a target for early intervention for AD. - Source: PubMed
Publication date: 2026/07/28
Liu CanWang XiangyuAn ChengGe ShenglinZhang Chengxin - Sickle cell disease (SCD) is a globally distributed hereditary red cell disorder with still high mortality. Growing evidence indicates that sickle cell related cardiovascular disease contributes to the early death of adults with SCD. Here, we show that humanized SCD mice developed an age-dependent cardiomyopathy characterized by (i) increased circulating Th17 lymphocytes, Th17 heart infiltration associated with increased plasma IL-17; (ii) collagen deposition and activation of both platelet derived growth factor-B (PDGF-B) and transforming growth factor-β1 (TGF-β1) canonical pathways; (iii) overactivation of heart NF-κB associated with up-regulation of NLRP3 and of inflammatory vasculopathy markers. We then used colchicine (CLC) that acts as anti-inflammatory drug with immunomodulatory effects. In humanized SCD mice, we demonstrated the protective role of low-dose CLC treatment against chronic inflammation and preserving myocardial performance. Of note, we found CLC also attenuating sickle cell related lung damage, suggesting a multiorgan effect of CLC in SCD mice. Our data generate the rationale to further explore CLC as new therapeutic tool to treat early stages of sickle cell cardiomyopathy. - Source: PubMed
Publication date: 2026/07/23
Iatcenko IanaFederti EnricaGhigo AlessandraCeolan JacopoPriolo RebeccaRecchiuti AntonioAndolfo ImmacolataIolascon AchilleMatte AlessandroPozzetto Huot RichardRiccardi VeronicaVillaboni SimoneMazzi FilippoTolosano EmanuelaGremese ElisaStella ManuelaForni Gian LucaDe Franceschi Lucia - Structural variants (SVs) are a major yet underused source of adaptive variation in aquaculture. We built a genome-wide SV atlas for 180 from six commercial breeding populations and discovered 1,159,046 SVs, with uneven chromosomal distributions and multi-type hotspots. Over 63.53% of SVs overlapped repeats-especially simple sequence repeats, DNA transposons, and LINEs. SV and SNP densities were highly correlated. Across populations, 482 k SVs were shared and 145,623 were singletons; the fraction of deletions increased from shared to singleton classes. BMK and KH harbored more singletons than SIS, RH, and CP, indicating greater divergence. PCA and ADMIXTURE recovered three major clusters and revealed the substructure in RH, mirroring SNP analyses. Selection scans identified 78-193 sweep windows per population encompassing 38-161 candidate genes. These genes were predominantly enriched in population-specific processes such as chromatin regulation, meiotic recombination, membrane-associated functions, suggesting that structural variants may contribute to divergence in reproductive, metabolic, and structural pathways across breeding programs. Nevertheless, 10 genes showed parallel signals in over 3 populations; many carry short deletions likely affecting regulatory or coding elements. Together, these results show that genome architecture and domestication jointly shape the shrimp SV landscape; that SVs alone robustly resolve population history; and that a small set of recurrent, deletion-bearing regulatory genes may underpin convergent improvement. The SV map and candidate loci provide diagnostic markers for germplasm tracing and candidate loci for marker-assisted or genomic selection in breeding. - Source: PubMed
Publication date: 2026/08/24
Zhao MingyangWang HaoTeng MingxuanLv HongyuZhao BaojunWang MengqiangBao ZhenminZeng Qifan