COVID-19 research: knock-out (KO) cell lines and lysates
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Save time with ready-made cell engineering products so you can get on with answering the bigger research questions.
Published 8th March 2021
Knock-out cell lines and lysates are essential reagents in understanding and further supporting the important research into COVID-19. Below is a curated list of high-quality, in-house manufactured knock-out products that enable you to confidently interrogate the relationship between genotype and phenotype without the complexity of creating gene-edited cell lines yourself.
Our ever-expanding catalog of COVID-19 related ready-made knock-out cell lines and lysates allows you to get your knock-out of choice in less than five days. All are easily accessible, increasingly relevant, and expertly made, providing you with a hassle-free solution.
Let Abcam's gene-edited cell lines help you get on with answering the bigger research questions.
COVID-19 related knock-outs
| Target and relation to COVID-19 | Image | KO cell line | KO cell lysate |
ACE2 ACE2 protects the lung and several other tissues from injury, given its role as a regulator of the renin-angiotensin system. It also acts as the cellular receptor for both SARS-CoV and SARS-CoV-2 (COVID-19). Due to the key role that ACE2 plays in host cell invasion by SARS-CoV-2, strategies are underway to develop drugs that can block this target. |
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ANPEP / CD13 Increased expression of the ectopeptidatase ANPEP/CD13 is a hallmark of inflammation. Therefore reduction of ANPEP activity has been investigated as a possible anti‐inflammatory therapy. ANPEP is a known receptor for coronaviruses, among them SARS-CoV-2 (COVID-19). Elevated ANPEP levels may contribute to the severity of SARS‐CoV‐2 infection and it has been speculated that it may be involved in the development of thrombocytopenia in patients with COVID-19. |  | ||
CD147 / BSG CD147, known as basigin or EMMPRIN, is a transmembrane glycoprotein involved in tumor development, and bacterial and virus infection. CD147 acts as a receptor for SARS-CoV-2 entry. Loss of CD147 or blocking CD147 by Meplazumab, an anti-CD147 humanized antibody, inhibits SARS-CoV-2 replication, whereas CD147 overexpression promotes virus infection, thus highlighting the potential of inhibiting CD147 as a target for COVID-19 treatment. |  | ||
CD74 Macrophage migration inhibitory factor (MIF) is a critical mediator of the host defense and is involved in both acute and chronic responses in the lung. CD74 forms part of the MIF receptor complex and it induces p44/p42 MAPK activation and MIF-mediated pulmonary inflammation. CD74 contributes to the adaptive immunity impairment in patients with COVID-19 and hence, CD74 and MIF may be potential targets to decrease neutrophilic lung inflammation and acute lung injury. Moreover, higher serum soluble CD74 levels may reflect the severity of lung injury and help physicians determine the prognosis of acute respiratory distress syndrome. |  | ||
CXCR5 CXCR5 is a major chemokine receptor mainly expressed on the surface of B cells and a subset of T cells. It binds to B-lymphocyte chemoattractant CXCL13 and is required for B cell homing. CXCL13 is found at a higher serum level in the severe COVID-19 patients than in the non-severe patients. CXCR5 expression is reduced on all major B cell subsets and non-naïve CD4 T cells in COVID-19 patients. |  | ||
IL-1 beta High levels of IL-1B together with IL-6 and IL-10 have been shown to drive airway inflammation in acute respiratory distress syndrome observed in some patients with COVID-19. |  | ||
IL-13 receptor alpha 2 IL13RA2 encodes the alpha-2 receptor subunit for interleukin-13 (IL-13). The IL-13 pathway has immunoregulatory functions and is implicated in several lung diseases. The IL-13 pathway can activate Janus kinase 2 (JAK2) and it has been shown that inhibition of JAK2 blocks SARS-CoV-2 viral entry. |  | ||
IL1RAP is required to activate IL-1 receptor signaling which is highly upregulated in patients with severe COVID-19 disease. |  | ||
IL-6 Systemic inflammation and respiratory failure in patients with COVID-19 are associated with increased release of cytokines, including IL-6. IL-6 may be used as a marker to predict respiratory failure, thus helping physicians correctly allocate patients at an early stage. Moreover, it is hypothesized that modulating the levels of IL-6 or its effects may alter the course of COVID-19. |  | ||
CXCL8 / IL-8 IL-8 has a potent role in the recruitment and activation of neutrophils, often elevated in patients with COVID-19. IL-8 is produced by lung epithelial cells upon infection and it is found to be highly expressed in patients with severe COVID-19 infection. |  | ||
CCL7 / MCP3 Bronchoalveolar fluid from patients with severe COVID-19 is enriched in CCL2 and CCL7, two chemokines that are the most potent at recruiting CCR2+ monocytes. Continuously high levels of CXCL10, CCL7, and IL-1 receptor antagonist cytokines in plasma of patients with COVID-19 are associated with increased viral load, loss of lung function, lung injury, and a fatal outcome. |  | ||
TNF alpha Increased inflammatory cytokines such as TNFα and IL-6 are observed in patients with COVID-19, especially in the severe group. Elevated IL-6 and TNF-α serum levels at presentation are strong predictors of disease severity and survival. |  |
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