SPARCL1 _ MAST9 Antibody (Antigen Affinity Purified)
- Known as:
- SPARCL1 _ MAST9 Antibody (Antigen Affinity Purified)
- Catalog number:
- 10046-RP01
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- SPARCL1 _ MAST9 Antibody (Antigen Affinity Purified)
Related genes to: SPARCL1 _ MAST9 Antibody (Antigen Affinity Purified)
- 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 _ MAST9 Antibody (Antigen Affinity Purified)
Related articles to: SPARCL1 _ MAST9 Antibody (Antigen Affinity Purified)
- The SPARC (secreted protein acidic and rich in cysteine) family represents a unique class of matricellular proteins - including SPARC, SPARCL1, SPOCK1-3, SMOC1-2, and FSTL1 - that regulate extracellular matrix (ECM) dynamics, cell signaling, and tissue homoeostasis. In cancer, their expression is frequently dysregulated, through epigenetic mechanisms, microRNAs, and interactions within the tumor microenvironment (TME). Dysregulation of SPARC family members is most pronounced in aggressive malignancies with SPARC, SPARCL1, SPOCK1, and SPOCK2 most consistently altered. These proteins drive tumor progression through ECM remodeling, epithelial-mesenchymal transition (EMT), maintenance of cancer stemness, immune modulation, and drug resistance acquisition. Their functions are highly context-dependent, exerting either tumor-suppressive or oncogenic effects depending on tissue types and disease stage. While their secreted nature positions family members as promising serum or plasma biomarkers, challenges such as ECM protein undruggability, functional heterogeneity, and the absence of upstream regulators have so far precluded direct therapeutic targeting, with no agents advancing to clinical trials. Nonetheless, indirect strategies leveraging their biology show preclinical promise. This review synthesizes current knowledge on SPARC family structure, regulation, and context-specific functions in cancer-TME interactions, emphasizing their dual roles as modulators of progression and resistance. By integrating mechanistic insights with translational advances, we highlight the emerging utility of SPARC family proteins in precision oncology and underscore the need for deeper understanding to enable effective biomarker development and targeted therapeutic strategies. - Source: PubMed
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Odden Michelle CLiu XiaojuanShah Amil MYang YiminLamberson VictoriaBrody Jennifer ASitlani Colleen MHuber MattKalani RizwanShojaie AliRaffield Laura MGlover LáShauntáPalta PriyaKucharska-Newton Anna MPsaty Bruce MFloyd James S - Osteoarthritis (OA) is a degenerative joint disease characterized by progressive cartilage breakdown and limited intrinsic repair capacity. Recent single-cell RNA sequencing (scRNA-seq) studies have revealed remarkable chondrocyte heterogeneity, identifying multiple functionally distinct subpopulations. Increasing evidence suggests that articular cartilage harbors progenitor-like chondrocytes with regenerative potential. - Source: PubMed
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Yan WeiningChu ZhilongQin KangCui ChengyuYu XiYan XinfengMa ChunxiaSun ShuiLi WeiLiang Weiqiang - Gastric cancer (GC) shows marked heterogeneity driven by the tumor microenvironment, leading to therapeutic resistance and poor prognosis. Using spatial transcriptomics of invasive murine tumors and human GC samples, we identified a distinct stromal-immune-vascular core region, termed the 'danger zone', which is enriched in diffuse-type GC and strongly linked to advanced stage and an immunosuppressive tumor microenvironment. Non-negative matrix factorization using danger zone signature genes stratified GC patients into two subtypes, with Subtype 2 exhibiting worse survival and impaired immunotherapy response. An XGBoost classifier based on 13 key genes-including CCDC80, MSRB3, FBLN1, and SPARCL1-accurately predicted subtypes and prognosis across cohorts. Single-cell and spatial analyses identified CCDC80 fibroblasts as key drivers within the danger zone. Mechanistically, CCDC80 fibroblasts recruit effector CD8 T cells through CXCL12-CXCR4 signaling and induce their dysfunction by markedly upregulating PD-1 and TIM-3, thereby promoting exhaustion and apoptosis. The interactions were validated using fibroblast-CD8 + T cell co-cultures and CXCL12 blockade. Finally, a LightGBM model predicted danger zone scores directly from H&E slides, correlating with stromal infiltration and patient survival. This study defines the danger zone as a key spatial feature of GC progression and immunosuppression, offering novel biomarkers, prognostic tools, and therapeutic targets. - Source: PubMed
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