SPARCL1 Antibody (Center) Blocking peptide
- Known as:
- SPARCL1 Antibody (Center) Blocking short protein sequence
- Catalog number:
- BP10208c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SPARCL1 Antibody (Center) Blocking peptide
Related genes to: SPARCL1 Antibody (Center) Blocking peptide
- Gene:
- SPARCL1 NIH gene
- Name:
- SPARC like 1
- Previous symbol:
- -
- Synonyms:
- MAST9
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2016-10-05
Related products to: SPARCL1 Antibody (Center) Blocking peptide
Related articles to: SPARCL1 Antibody (Center) Blocking peptide
- Bone fractures in Thoroughbred racehorses are a major welfare problem. Genetic factors contribute to fracture risk. Cell models have previously identified 112 differentially expressed genes in bone-forming osteoblasts derived from horses at high and low genetic risk of fracture. However, 42 of these genes have no published role in bone. In this study, we identified novel roles for a subset of these genes in bone formation. Twenty-six of the 42 genes were expressed in Saos2 cells during basal culture and/or after 21 days of osteogenic culture. Five of these genes (ADSSL1, CABP1, ENO2, SPARCL1 and UCP2) were then stably overexpressed and knocked down, and their effect on osteogenesis was measured. Gene overexpression resulted in significant decreases in Saos2 cell viability and decreased expression of osteogenic genes under basal cell culture, but after 21 days of osteogenic culture there were few significant changes in osteogenic gene expression, collagen deposition or matrix mineralisation. Knockdown of SPARCL1 resulted in total cell death, whereas knockdown of ADSSL1, CABP1, ENO2 and UCP2 resulted in decreased cell viability but limited significant changes in osteogenic gene expression under basal cell culture. However, following osteogenic culture, gene knockdown induced widespread changes in osteogenic gene expression, decreased collagen deposition and increased matrix mineralisation. ADSSL1, CABP1, ENO2 and UCP2 were all expressed at significantly lower levels in osteoblasts from genetically high-risk horses. Taken together, this work demonstrates novel roles for fracture-associated genes in bone formation and matrix mineralisation suggesting these processes may be altered in genetically susceptible horses. - Source: PubMed
Ross Amy CLumsden Ellison SFlood CarolineDudhia JayeshPsifidi AndronikiGuest Deborah J - Vascular dementia (VaD) is a prevalent age-related neurocognitive disorder characterized by progressive cognitive impairment and a lack of disease-modifying therapies. Although age-related brain endothelial dysfunction has been implicated as a central contributor to the pathogenesis of VaD, the molecular mechanisms underlying this process remain incompletely elucidated. - Source: PubMed
Publication date: 2026/06/29
Jin JianchengXu QiuhanPeng GuotaoZhou JiankuaiLiu YuchunMo Jun - Post-COVID-19 condition (PCC) is often accompanied by endocrine and immune dysregulation. Growth hormone (GH)deficiency has been reported in PCC patients, but its systemic effects remain poorly defined. - Source: PubMed
Publication date: 2026/06/03
Bai GuirongXie XiaominLi ShitingJi WenruiLi HuanHe YantingZhang LiLi LingPei SiqiYang YazhiWu YawenPing Rui - Papillary thyroid carcinoma (PTC) is the most prevalent type of thyroid malignancy, where invasive growth and distant metastasis contribute to a worsened patient prognosis. SPARCL1, a known tumor suppressor gene in various cancers, encodes a secreted glycoprotein. Preliminary research suggests that elevated expression of SPARCL1 is correlated with a better prognosis in PTC, highlighting its potential as an innovative restorative therapeutic agent, but its specific role and underlying mechanisms remain unclear. This study aimed to investigate the impact of SPARCL1 on the invasion and metastasis of PTC cells by constructing an overexpression model of SPARCL1 in PTC cells through viral transduction, collecting the supernatant proteins from the PTC cell model and adding them to PTC cells, and introducing recombinant SPARCL1 protein into PTC cells. In addition, we conducted animal experiments to detect the effects of SPARCL1 on the subcutaneous tumor formation and multi-organ metastasis of PTC cells in mice, as well as the inhibitory effect of recombinant SPARCL1 on tumors formed by PTC cells. The findings revealed that overexpression of the SPARCL1 gene, the secretory form of the SPARCL1 protein, and the recombinant SPARCL1 protein all significantly inhibited the malignant biological behaviors of PTC cells. Overexpression of SPARCL1 can inhibit the subcutaneous growth of tumor cells and their metastasis to the lungs, liver, and kidneys of mice, and recombinant SPARCL1 protein can also inhibit the growth of subcutaneous tumors. Mechanistically, SPARCL1 appears to mediate its anti-tumor effects through the SLC3A2-mediated ferroptosis pathway, suggesting a novel mechanism by which SPARCL1 influences PTC progression. In summary, SPARCL1 inhibits the proliferation, invasion, and metastasis of PTC, highlighting its potential as a candidate for innovative restorative therapies in PTC treatment. - Source: PubMed
Publication date: 2026/06/08
Wu FengpingZhang JinkangZhang XiaoliXu DongkunCheng ShuanghuaLiu QianGan YuxinRen LifangYang HaochengZhang KunXia XuliangJiang ZhiqiangShi YuhongTu Wenling - Bone metastasis is a leading cause of death in prostate cancer (PC) patients. Although androgen deprivation therapy (ADT) combined with novel androgen-targeted agents constitutes the cornerstone of systemic treatment, its efficacy is limited. We investigated the adrenal contribution to promoting progression of castration-resistant PC (CRPC) within bone using a preclinical intratibial xenograft model (VCaP, 22Rv1, and LNCaP cells). Mice underwent orchiectomy (ORX) to mimic ADT, with or without adrenalectomy (ORX + ADX) to eliminate adrenal contribution. A significant increase in bone mineral density (BMD) was observed in tumor-grafted tibiae in ORX-treated mice compared with controls (P < 0.001), indicating a strong tumor-induced sclerotic response. In contrast, ORX + ADX reduced tumor take rate by approximately 50% and decreased tumor-induced BMD by over 80% (P < 0.001). Transcriptomic analysis revealed that ADX downregulated tumor-induced transcripts in bone by over 90%, including osteogenic (Lox, Sparcl1, Bmp2, Postn, and Col1a1) and pro-angiogenic (Bmper, Pecam-1, and Esam) signatures. In addition, BMP, PI3K/Akt, and ERK1/2 signaling pathways were associated with the tumor-induced bone response. Both high serum progesterone and intratumoral levels of dihydrotestosterone (DHT) were associated with the sclerotic bone phenotype. ADX markedly reduced intratumoral DHT and downregulated glycolytic genes (HK2, PFK2, and LDHA) and secretory proteins expressed by the tumor, including stanniocalcin 2, potentially mediating paracrine effects in the sclerotic bone response. Altogether, these findings highlight the critical role of adrenal-dependent androgen synthesis, particularly via progesterone, in driving the sclerotic CRPC in bone. Our findings suggest that a comprehensive blockade of adrenal contribution is essential to prevent the sclerotic bone response associated with CRPC. - Source: PubMed
Publication date: 2026/06/09
Hagberg Thulin MalinLi LeiAbrahamsson SannaLandin AndreasHorkeby KarinWu JianyaoLagerquist Marie KOhlsson ClaesPoutanen Matti