Certificate of Analysis 1.05581 HX99182381
- Document Type:
- Certificate of Analysis
- Lot Number:
- HX99182381
- Product Catalog Number:
- 1.05581
146076mm
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Certificate of Analysis 1.05581 HX183290
- Document Type:
- Certificate of Analysis
- Lot Number:
- HX183290
- Product Catalog Number:
- 1.05581
-
Certificate of Analysis 1.05581 HX74336781
- Document Type:
- Certificate of Analysis
- Lot Number:
- HX74336781
- Product Catalog Number:
- 1.05581
-
Certificate of Analysis 1.05581 HX87991681
- Document Type:
- Certificate of Analysis
- Lot Number:
- HX87991681
- Product Catalog Number:
- 1.05581
-
Certificate of Analysis 1.05581 HX68746581
- Document Type:
- Certificate of Analysis
- Lot Number:
- HX68746581
- Product Catalog Number:
- 1.05581
-
COA 105581
- Document Type:
- Certificate of Analysis
- Product Catalog Number:
- 105581
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Epigenetic memory at malaria virulence genes.
- During its red blood cell stage, the malaria parasite Plasmodium falciparum can switch its variant surface proteins (P. falciparum erythrocyte membrane protein 1) to evade the host immune response. The var gene family encodes P. falciparum erythrocyte membrane protein 1, different versions of which have unique binding specificities to various human endothelial surface molecules. Individual parasites each contain approximately 60 var genes at various locations within their chromosomes; however, parasite isolates contain different complements of var genes, thus, the gene family is enormous with a virtually unlimited number of members. A single var gene is expressed by each parasite in a mutually exclusive manner. We report that control of var gene transcription and antigenic variation is associated with a chromatin memory that includes methylation of histone H3 at lysine K9 as an epigenetic mark. We also discuss how gene transcription memory may affect the mechanism of pathogenesis and immune evasion.
- Document Type:
- Reference
- Product Catalog Number:
- Multiple
- Product Catalog Name:
- Multiple
-
Analysis of CFTR folding and degradation in transiently transfected cells.
- Misfolding and premature degradation of F508del-CFTR is the major cause of cystic fibrosis. Components of the ubiquitin-proteasome system function on the surface of the endoplasmic reticulum to select misfolded proteins for degradation. The folding status of F508del-CFTR is monitored by at least two ER quality control checkpoints. The ER-associated Derlin-1/RMA1 E3 complex appears to recognize folding defects in CFTR that involve misassembly of NBD1 into a complex with the R-domain. In contrast, the cytosolic Hsp70/CHIP E3 complex appears to sense folding defects that occur after synthesis of NBD2. Herein we describe methods that allow for the study of how modulation of these ER quality control factors by siRNA impacts CFTR folding and degradation. The experimental system described employs transiently transfected HEK293 cells and is utilized to monitor the biogenesis of CFTR by both Western blot and pulse chase studies. Methods to detect complexes formed between CFTR folding intermediates and ER quality control factors will also be described.
- Document Type:
- Reference
- Product Catalog Number:
- 05-581
- Product Catalog Name:
- Anti-CFTR Antibody, clone MM13-4
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Fast and Precise. Thin Layer Chromatography by.
- Document Type:
- Brochure
- Product Catalog Number:
- Multiple
- Product Catalog Name:
- Multiple