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Human Laminin 521 Protein, premium grade

产品描述(Product Details)

Laminin 521 (LN521) is a recombinant human protein that provides a defined surface for in vitro feeder-free culture of multiple human pluripotent stem cells (PSCs). LN521 has been proven to maintain normal growth characteristics and stemness in multiple PSC lines without simultaneous differentiation, which includes ESC, iPSC, MSC etc. In addition, LN521 has been demonstrated to support PSC growth for >10 passages without any signs of karyotypic abnormalities and to maintain the ability of PSCs to differentiate into all three germ line lineages.
We have different versions of laminin 521 protein. In most applications, laminin 521 protein (LA5-H5261) has similar performance with laminin 521 protein (LA5-H5214). However, there might be slight difference in specific applications, so it is recommended to try these two products and choose the best product.

Flexible & Compatible
Laminin 521 could work well in any commercial stem cell media. Meanwhile, it could support the attachment and expansion of hPSCs both in single cells or small colonies.

Stemness maintenance
Laminin 521 is the biologically relevant hPSCs extracellular matrix. It is crucial for the growth and stemness maintenance of hPSCs in human through its binding to cell receptors a6β1 integrin.

Enhance cell differentiation
Due to the diverse biorelevant environment, laminin 521 could also enhance cell differentiation, polarization and organization of target cell types, including neuron, hepatocytes, cardiomyocytes, retinal pigmented epithelial cells, pancreatic β-cells and so on.

Reduce Variability
LN521 is a defined, recombinant human protein with better lot-to-lot consistency that reduces variability in your PSC cultures.

产品参数(Key parameter)

Purity (SDS PAGE)> 95%
Mycoplasma TestNegative
Sterility TestNegative
Endotoxin Test< 0.01 EU per μg
Host Cell Protein< 0.5 ng/µg
Host Cell DNA< 0.02 ng/μg

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

Contact us for customized product form or formulation.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 24 months in lyophilized state;
  2. -70°C for 12 months under sterile conditions after reconstitution;
  3. 2-8°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

活性(Bioactivity)-SPR

Laminin 521 SPR

Human Laminin 521 Protein, premium grade (Cat. No. LA5-H5214) immobilized on CM5 Chip can bind Human ITGA6&ITGB1 Heterodimer Protein, His Tag&Tag Free (IT1-H52W7) with an affinity constant of 19.9 nM as determined in a SPR assay (Biacore 8K) (QC tested).

Protocol

 
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前沿进展

The Loss of HJV Aggravates Muscle Atrophy by Promoting the Activation of the TβRII/Smad3 Pathway
Wang, Tao, Jia et al
Int J Mol Sci (2025) 26 (5)
Abstract: Hemojuvelin (HJV) is a membrane-bound protein prominently expressed in the skeletal muscle, heart, and liver. Despite its established function in iron regulation, the specific role of HJV in muscle physiology and pathophysiology is not well understood. In this study, we explored the involvement of HJV in disuse-induced muscle atrophy and uncovered the potential mechanisms. Hindlimb unloading (HU) resulted in soleus muscle atrophy in wild type (WT) mice, accompanied by a significant decrease in HJV protein expression. The muscle-specific deletion of Hjv (MKO) exacerbated myofiber atrophy, which was associated with an increase in the expression of muscle ubiquitin ligases following HU. Furthermore, the expression of transforming growth factor-β type II receptor (TβRII) and the level of phosphorylated Smad3 (p-Smad3) were elevated after HU, and these effects were exacerbated in MKO mice. The knockdown of TβRII in the skeletal muscle of MKO mice mitigated myofiber atrophy and reversed the hyperactivation of the TβRII/Smad3 pathway induced by HU. Our findings demonstrate that the absence of HJV contributes to the activation of the TβRII/Smad3 signaling pathway and, consequently, the onset of myofiber atrophy in response to HU. Given its abundant expression in skeletal muscle, HJV emerges as a potential therapeutic target for muscle atrophy.
Identification of 8-(2-methyl phenyl)-9H-benzo[f]indeno[2,1-c]quinolin-9-one (C-5635020) as a novel and selective TGFβ RII kinase inhibitor for breast cancer therapy
Al Shahrani, Abohassan, Alshahrani et al
Biochem Biophys Res Commun (2025) 746, 151225
Abstract: Transforming growth factor-beta (TGF-β) plays a pivotal role in breast development by modulating tissue composition during the developmental phase. The TGFβ type II receptor (TGFβ RII) is implicated in breast cancer and represents a valuable therapeutic target. Due to the off-target side effects of many existing TGFβI/TGFβ RII inhibitors, a more targeted approach to drug discovery is necessary. This study used computational modeling and molecular dynamics simulations to screen the ChemBridge small molecule library against TGFβ RII.This study employed high-throughput virtual screening, molecular dynamics simulations, and binding free energy calculations to identify potential inhibitors targeting TGF-β RII. MDA-MB 231 and MCF-7 breast cancer cells were used in anti-proliferative, tans-endothelial migration, and flow cytometric assays for in vitro validations.We identified 8-(2-methylphenyl)-9H-benzo[f]indeno[2,1-c]quinolin-9-one (C-5635020) as a potent and selective inhibitor. Protein-ligand modeling analysis revealed that C-5635020 targets the kinase domain of TGFβ RII with superior binding affinities compared to the standard drug, staurosporine. Computational results suggest that C-5635020 selectively binds and inhibits TGFβ RII activity, thereby controlling cell proliferation in breast cancer. In vitro, experiments corroborated these predictions, where C-5635020 inhibited TGFβ RII and p-Smad 2/3 positive population in MDAMB-231 and MCF-7 cells. The compound dose-dependently inhibited cell proliferation, trans-endothelial migration, and increased apoptosis in both breast cancer cell lines.The strong binding affinity, stability, and favorable thermodynamics of C-5635020 with established in vitro efficacy highlight its potential as a lead compound for further preclinical and clinical developments for breast cancer treatment.Copyright © 2024. Published by Elsevier Inc.
The Role of TGF-β1 and Mutant SMAD4 on Epithelial-Mesenchymal Transition Features in Head and Neck Squamous Cell Carcinoma Cell Lines
Bette, Reinhardt, Gansukh et al
Cancers (Basel) (2024) 16 (18)
Abstract: The aim of the present study was to investigate possible differences in the sensitivity of HNSCC cells to known EMT regulators. Three HNSCC cell lines (UM-SCC-1, -3, -22B) and the HaCaT control keratinocyte cell line were exposed to transforming growth factor beta 1 (TGF-β1), a known EMT master regulator, and the cellular response was evaluated by real-time cell analysis (RTCA), Western blot, quantitative PCR, flow cytometry, immunocytochemistry, and the wound closure (scratch) assay. Targeted sequencing on 50 cancer-related genes was performed using the Cancer Hotspot Panel v2. Mutant, and wild type SMAD4 cDNA was used to generate recombinant SMAD4 constructs for expression in mammalian cell lines. The most extensive response to TGF-β1, such as cell growth and migration, β-actin expression, or E-cadherin (CDH1) downregulation, was seen in cells with a more epithelial phenotype. Lower response correlated with higher basal p-TGFβ RII (Tyr424) levels, pointing to a possible autocrine pre-activation of these cell lines. Targeted sequencing revealed a homozygous SMAD4 mutation in the UM-SCC-22B cell line. Furthermore, PCR cloning of SMAD4 cDNA from the same cell line revealed an additional SMAD4 transcript with a 14 bp insertion mutation, which gives rise to a truncated SMAD4 protein. Overexpression of this mutant SMAD4 protein in the highly epithelial control cell line HaCaT resulted in upregulation of TGF-β1 and vimentin. Consistent with previous reports, the invasive and metastatic potential of HNSCC tumor cells appears associated with the level of autocrine secretion of EMT regulators such as TGF-β1, and it could be influenced by exogenous EMT cytokines such as those derived from immune cells of the tumor microenvironment. Furthermore, mutant SMAD4 appears to be a significant contributor to the mesenchymal transformation of HNSCC cells.
Expression and Transcriptional Targets of TGFβ-RII in Paracentrotus lividus Larval Skeletogenesis
Goloe, Gildor, Ben-Tabou de-Leon
Genesis (2024) 62 (4), e23614
Abstract: Organisms from the five kingdoms of life use minerals to harden their tissues and make teeth, shells and skeletons, in the process of biomineralization. The sea urchin larval skeleton is an excellent system to study the biological regulation of biomineralization and its evolution. The gene regulatory network (GRN) that controls sea urchin skeletogenesis is known in great details and shows similarity to the GRN that controls vertebrates' vascularization while it is quite distinct from the GRN that drives vertebrates' bone formation. Yet, transforming growth factor beta (TGF-β) signaling regulates both sea urchin and vertebrates' skeletogenesis. Here, we study the upstream regulation and identify transcriptional targets of TGF-β in the Mediterranean Sea urchin species, Paracentrotus lividus. TGF-βRII is transiently active in the skeletogenic cells downstream of vascular endothelial growth factor (VEGF) signaling, in P. lividus. Continuous perturbation of TGF-βRII activity significantly impairs skeletal elongation and the expression of key skeletogenic genes. Perturbation of TGF-βRII after skeletal initiation leads to a delay in skeletal elongation and minor changes in gene expression. TGF-β targets are distinct from its transcriptional targets during vertebrates' bone formation, suggesting that the role of TGF-β in biomineralization in these two phyla results from convergent evolution.© 2024 The Author(s). genesis published by Wiley Periodicals LLC.
Showing 1-4 of 668 papers.
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