Factor B Knockout
Factor B Knockout - Related Videos
11:53
A Protocol for Multiple Gene Knockout in Mouse Small Intestinal Organoids Using a CRISPR-concatemer
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Cited by 17 •
2017
This protocol describes the steps for cloning multiple single guide RNAs into one guide RNA concatemer vector, which is of particular use in creating multi-gene knockouts using CRISPR/Cas9 technology. The generation of double knockouts in intestinal organoids is shown as a possible application of this method.
10:59
Production of Apolipoprotein C-III Knockout Rabbits using Zinc Finger Nucleases
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Cited by 32 •
2013
Recent development in gene targeting tools makes production of knockout (KO) rabbits possible. In the present work, we generated five Apolipoprotein (Apo) C-III KO rabbits using Zinc Finger Nucleases (ZFN). This work demonstrated that ZFN is a highly efficient method to produce KO rabbits.
04:13
CRISPR Concatemer-Mediated Multiple Gene Knockout: A Technique to Simultaneously Knockout Multiple Genes by Non-Homologous End-Joining Pathway in Mouse Intestinal Cells
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2025
This video describes a gene knockout technique using a CRISPR-concatemer to simultaneously knock out multiple genes in cultured mouse intestinal organoid cells. This method is used to knock out a diseased gene and to elucidate the function of a gene and its paralogues.
11:35
Selection-dependent and Independent Generation of CRISPR/Cas9-mediated Gene Knockouts in Mammalian Cells
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Cited by 6 •
2017
Recent advances in the ability to genetically manipulate somatic cell lines hold great potential for basic and applied research. Here, we present two approaches for CRISPR/Cas9 generated knockout production and screening in mammalian cell lines, with and without the use of selectable markers.
02:29
In-vitro Mutagenesis (Gene Knockouts)
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2026
To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes. The Process Genes can be randomly knocked out, or specific genes can be targeted. To knock out a particular gene, an engineered piece of DNA called a targeting vector is used to replace the...
FAQs
Factor B loss interferes with spontaneous C3 convertase formation, a key initiating and amplification step in the alternative complement pathway. As a result, the pathway has reduced capacity to sustain downstream complement activation. This helps investigators determine how much complement activity depends on alternative-pathway amplification rather than on activation initiated through the classical or lectin pathways.
The model selectively weakens alternative-pathway function while leaving the classical and lectin pathways available for comparison. Differences observed between Factor B-deficient and appropriate comparator systems can therefore indicate processes that require alternative-pathway activity. This distinction is especially useful when studying whether complement-dependent effects arise from pathway-specific amplification or from broader complement activation.
Reduced alternative-pathway activity can decrease downstream complement effects, including opsonization and membrane attack complex formation. These changes may alter how immune systems interact with infectious agents and may also influence inflammatory responses or tissue injury. The model therefore connects a defined complement defect with both protective outcomes, such as pathogen clearance, and potentially damaging immune consequences.
Interpretation should focus on outcomes in the Factor B-deficient condition relative to systems that retain Factor B, while considering the contributions of the classical and lectin pathways. Changes in complement activation, opsonization, membrane attack complex formation, pathogen clearance, inflammation, or tissue injury can then be evaluated for their relationship to alternative-pathway function rather than treated as effects of complement loss in general.
In infection studies, the model can reveal whether alternative-pathway activity contributes to pathogen clearance and related immune responses. Researchers can examine how removing Factor B changes complement-dependent interactions with infectious agents and whether remaining pathways compensate for the deficiency. These comparisons help define the role of alternative-pathway amplification in host defense and infection-associated inflammation.
Factor B knockout provides a way to examine consequences of eliminating alternative-pathway function before considering therapeutic targeting of that pathway. Observed changes in complement activation, pathogen clearance, inflammatory responses, or tissue injury can identify processes that may be influenced by Factor B-dependent activity. The findings can also help distinguish potentially protective complement effects from effects associated with immune-mediated damage.