CRISPR Delivered to Cells: Methods and Mechanisms

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-08-11

Introduction to CRISPR Delivery

What is CRISPR?

CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) is an adaptive immune system found naturally in bacteria and archaea. The most widely used variant for genome editing is the CRISPR-Cas9 system, derived from Streptococcus pyogenes. In its functional form, the system comprises two core components: the Cas9 endonuclease, a 160 kDa protein that creates double-strand breaks (DSBs) in DNA, and a single guide RNA (sgRNA), a ~100-nucleotide RNA molecule that directs Cas9 to a specific genomic locus via Watson-Crick base pairing. The sgRNA contains a 20-nucleotide spacer sequence complementary to the target DNA, followed by a scaffold region that binds Cas9. For Cas9 to cleave, the target sequence must be immediately followed by a protospacer adjacent motif (PAM), which for S. pyogenes Cas9 is 5′-NGG-3′. Upon binding, Cas9 generates a blunt DSB three base pairs upstream of the PAM. The cell then repairs this break either through non-homologous end joining (NHEJ), which typically introduces small insertions or deletions (indels) that disrupt the gene, or through homology-directed repair (HDR), which can introduce a donor template sequence. For a deeper mechanistic overview of the nuclease itself, see CRISPR Cas 9.

Why Delivery Matters

The delivery of CRISPR components into cells is the single most critical logistical step in any genome editing experiment. A well-designed sgRNA and a functional Cas9 enzyme are useless if they never reach the nucleus of the target cell. Delivery is not merely a matter of getting molecules across the plasma membrane; it also involves ensuring that the components survive intracellular nucleases, escape endosomal compartments, and translocate into the nucleus. The method chosen determines the duration of Cas9 expression, the level of editing efficiency, the degree of off-target activity, and the viability of the treated cells. In practical terms, delivery is the difference between a clean, reproducible knockout and a failed experiment. For applications such as CRISPR Knockout or CRISPR Knock experiments, the delivery route must be matched to the desired outcome—transient disruption versus stable modification.

Forms of CRISPR Components for Delivery

CRISPR components can be delivered in three distinct molecular formats: plasmid DNA, mRNA, or ribonucleoprotein (RNP) complexes. Each format has distinct pharmacokinetic properties, cost profiles, and experimental implications.

Plasmid DNA

Plasmids are circular, double-stranded DNA molecules that encode both Cas9 and the sgRNA under the control of eukaryotic promoters. The Cas9 gene is typically driven by a strong constitutive promoter such as the cytomegalovirus (CMV) immediate-early promoter or the chicken β-actin (CBA) promoter. The sgRNA is expressed from a RNA polymerase III promoter, most commonly the human U6 promoter, which produces a precisely defined transcript without a 5′ cap or 3′ poly(A) tail.

Advantages: Plasmids are inexpensive to produce in large quantities using standard bacterial culture. They are stable at −20 °C for years. They allow for the inclusion of additional elements, such as antibiotic resistance markers for stable selection or fluorescent reporter genes for tracking transfected cells.

Disadvantages: Plasmid delivery requires transcription and translation before active Cas9 protein exists, introducing a delay of 12–24 hours. The DNA must traverse the nuclear envelope, which is only permeable during mitosis; non-dividing cells are therefore refractory to plasmid-based editing. Plasmids persist in the cell for days to weeks, leading to prolonged Cas9 expression, which increases off-target editing. There is also a small but real risk of random integration of plasmid fragments into the host genome.

mRNA

In this format, the Cas9 coding sequence is transcribed in vitro into messenger RNA, typically with a 5′ cap analog (e.g., CleanCap) and a 3′ poly(A) tail to enhance stability and translation. The sgRNA is delivered separately, either as a chemically synthesized RNA or as an in vitro transcribed transcript.

Advantages: mRNA is translated directly in the cytoplasm, so editing begins sooner than with plasmid DNA. Because mRNA does not need to enter the nucleus for expression, it works in non-dividing cells. The mRNA is degraded by endogenous RNases within 24–72 hours, resulting in a transient pulse of Cas9 activity that reduces off-target effects.

Disadvantages: mRNA is labile and requires careful handling, including RNase-free conditions and storage at −80 °C. It is more expensive to produce than plasmid DNA. The requirement for two separate RNA molecules (Cas9 mRNA and sgRNA) increases the complexity of co-delivery.

Ribonucleoprotein (RNP)

The RNP complex is a pre-assembled complex of recombinant Cas9 protein and chemically synthesized sgRNA. The two components are mixed in vitro, typically in a 1:1.2 molar ratio (Cas9:sgRNA), and incubated at room temperature for 10 minutes to allow complex formation. The RNP is then delivered directly into cells.

Advantages: RNP delivery is the fastest route to editing because no transcription or translation is required. The Cas9 protein is degraded by cellular proteases within 24–48 hours, providing the shortest window of activity and the lowest off-target rates. RNP delivery completely avoids the risk of DNA integration. It is also the most reproducible format, as the stoichiometry is precisely controlled.

Disadvantages: Recombinant Cas9 protein is expensive to produce and purify. RNPs are large (~160 kDa protein plus ~30 kDa RNA) and do not readily cross cell membranes, necessitating physical or chemical delivery methods. The complex is sensitive to freeze-thaw cycles and must be stored at −80 °C in a buffered solution containing glycerol.

Viral Delivery Methods

Viral vectors exploit the natural ability of viruses to enter cells and deliver genetic cargo. Three viral systems dominate CRISPR delivery: adeno-associated virus (AAV), lentivirus, and adenovirus.

Adeno-Associated Virus (AAV)

AAV is a small (~25 nm), non-enveloped, single-stranded DNA virus from the Parvoviridae family. It is non-pathogenic in humans and requires a helper virus (adenovirus or herpesvirus) for replication, which makes it a safe delivery vehicle. Recombinant AAV (rAAV) vectors retain only the two inverted terminal repeats (ITRs) of the viral genome, removing all viral coding sequences.

Cargo capacity: The major limitation of AAV is its packaging capacity of approximately 4.7 kb. The S. pyogenes Cas9 coding sequence alone is 4.2 kb, leaving insufficient room for the sgRNA expression cassette and regulatory elements. Several strategies circumvent this:

1. Split-Cas9: The Cas9 gene is split into two halves, each packaged in a separate AAV vector. Upon co-infection, the two halves are reconstituted via intein-mediated protein splicing.
2. Smaller Cas9 orthologs: Staphylococcus aureus Cas9 (SaCas9) is 3.2 kb and fits alongside an sgRNA cassette within a single AAV vector.
3. Dual-vector systems: One AAV carries the Cas9 gene, and a second carries the sgRNA and a donor template for HDR.

Advantages: AAV transduces both dividing and non-dividing cells, achieves long-term expression in post-mitotic tissues, and elicits a minimal immune response. Serotypes such as AAV2, AAV6, and AAV9 have distinct tissue tropisms, allowing some targeting specificity.

Disadvantages: The small cargo capacity is a significant constraint. AAV genomes remain predominantly episomal, but integration at the AAVS1 locus on chromosome 19 occurs at a low frequency. Pre-existing neutralizing antibodies against AAV capsids in humans can block transduction.

Lentivirus

Lentiviruses are a genus of retroviruses that include HIV-1. Recombinant lentiviral vectors are pseudotyped with the vesicular stomatitis virus G glycoprotein (VSV-G), which broadens tropism and enhances particle stability. Lentiviral vectors integrate their cargo into the host genome, providing stable, heritable expression.

Cargo capacity: Lentiviral vectors can accommodate inserts up to 8–10 kb, sufficient for a full Cas9 expression cassette plus an sgRNA and a selection marker. This makes them ideal for generating stable cell lines with constitutive or inducible Cas9 expression.

Advantages: Lentiviral delivery achieves stable integration, which is essential for long-term experiments such as pooled CRISPR screens. The system transduces both dividing and non-dividing cells.

Disadvantages: Random genomic integration carries the risk of insertional mutagenesis, potentially disrupting tumor suppressor genes or activating oncogenes. This is a particular concern for therapeutic applications. The prolonged expression of Cas9 from an integrated cassette increases off-target editing. Lentiviral production requires biosafety level 2 (BSL-2) facilities.

Adenovirus

Adenoviruses are non-enveloped, double-stranded DNA viruses with a ~36 kb genome. First-generation adenoviral vectors delete the E1 and E3 regions, creating a cargo capacity of approximately 8 kb. The viral genome remains episomal, so there is no risk of insertional mutagenesis.

Advantages: Adenoviral vectors achieve high transduction efficiency in a broad range of cell types, including primary cells. They do not integrate into the host genome, and the cargo is lost over time as cells divide, providing a transient expression profile.

Disadvantages: Adenoviruses elicit a strong innate and adaptive immune response, which limits their use in vivo. The episomal genome is diluted out in dividing cells, making adenovirus unsuitable for stable expression experiments. High doses can cause cytotoxicity.

Non-Viral Delivery Methods

Non-viral methods avoid the immunogenicity and insertional mutagenesis risks of viral vectors. They are generally cheaper and easier to scale, but often achieve lower delivery efficiency.

Lipid Nanoparticles (LNPs)

Lipid nanoparticles are spherical vesicles composed of ionizable cationic lipids, phospholipids, cholesterol, and polyethylene glycol (PEG)-lipid conjugates. The ionizable lipids are positively charged at acidic pH, which facilitates encapsulation of negatively charged nucleic acids during formulation, but neutral at physiological pH, reducing toxicity.

Mechanism of action: LNPs enter cells primarily through clathrin-mediated endocytosis. Once inside the endosome, the acidic environment protonates the ionizable lipids, promoting fusion between the LNP and the endosomal membrane. This releases the cargo into the cytoplasm—a process termed the "proton sponge" effect, though the precise mechanism remains debated.

Applications: LNPs are the leading non-viral platform for mRNA delivery. The FDA-approved mRNA vaccines for SARS-CoV-2 use this technology. For CRISPR, LNPs are typically used to deliver Cas9 mRNA or RNP complexes. The sgRNA can be co-encapsulated or chemically modified for stability.

Advantages: LNPs are highly efficient for mRNA delivery, are biodegradable, and can be functionalized with targeting ligands (e.g., antibodies or peptides) for cell-specific delivery. They are also suitable for systemic administration in vivo.

Disadvantages: LNP formulation is technically demanding and requires microfluidic mixing devices for reproducible particle size. LNPs accumulate primarily in the liver after intravenous injection, limiting delivery to other tissues. Endosomal escape is inefficient—only a small fraction of internalized cargo reaches the cytoplasm.

Polymer-Based Delivery

Cationic polymers, such as polyethyleneimine (PEI) and poly(L-lysine) (PLL), condense nucleic acids into polyplexes through electrostatic interactions. PEI is the most widely used polymer for in vitro transfection.

Mechanism: PEI has a high density of primary, secondary, and tertiary amines, giving it a strong buffering capacity. This property is thought to facilitate endosomal escape via the proton sponge effect, where the polymer absorbs protons as the endosome acidifies, causing osmotic swelling and vesicle rupture.

Advantages: Polymers are inexpensive, easy to modify, and can be conjugated to targeting moieties. PEI is effective for plasmid DNA delivery in many cell lines.

Disadvantages: PEI is cytotoxic at the concentrations required for high transfection efficiency. The polyplexes are heterogeneous in size and can aggregate in serum-containing media. Delivery efficiency varies widely between cell types, and polymers are generally less effective for RNP delivery than for DNA.

Other Chemical Methods

Calcium phosphate transfection: DNA is precipitated with calcium phosphate and the precipitate is taken up by cells via endocytosis. This method is inexpensive and works well for adherent cell lines, but efficiency is low and highly pH-sensitive.

DEAE-dextran: A cationic polysaccharide that complexes with DNA. It is less toxic than PEI but has lower transfection efficiency and is limited to certain cell types.

Cell-penetrating peptides (CPPs): Short cationic or amphipathic peptides (e.g., TAT from HIV-1, penetratin) that can carry cargo across the plasma membrane. CPPs have been used to deliver Cas9 protein and RNPs, but efficiency is variable and the mechanism of uptake is incompletely understood.

Physical Delivery Methods

Physical methods bypass the need for chemical carriers by directly introducing CRISPR components through mechanical or electrical means.

Electroporation

Electroporation applies a brief, high-voltage electrical pulse to cells, creating transient pores in the plasma membrane through which nucleic acids or proteins can enter. The technique is performed in a specialized cuvette or multi-well plate with electrodes.

Protocol outline:

1. Harvest cells and wash in a low-conductivity buffer (e.g., phosphate-buffered sucrose).
2. Resuspend cells at a density of 1–5 × 10⁶ cells/mL in electroporation buffer.
3. Add CRISPR components (plasmid, mRNA, or RNP).
4. Apply an exponential decay or square-wave pulse. Typical parameters for mammalian cells: 100–300 V, 25 µF capacitance, 1–5 ms pulse duration.
5. Immediately transfer cells to pre-warmed culture medium.

Advantages: Electroporation achieves high delivery efficiency in a wide range of cell types, including primary cells and hard-to-transfect cells such as T lymphocytes and hematopoietic stem cells. It is the method of choice for RNP delivery because the large protein-RNA complex does not need to cross a lipid bilayer on its own.

Disadvantages: Electroporation causes significant cell death, typically 20–50% depending on cell type and pulse parameters. The procedure requires specialized equipment and optimization of voltage, capacitance, and cell density. For applications involving CRISPR in T Cells, electroporation is the standard approach, but the associated toxicity must be carefully managed.

Microinjection

Microinjection uses a fine glass needle (0.5–1.0 µm tip diameter) to physically inject CRISPR components directly into the cytoplasm or nucleus of individual cells. This is performed under a microscope using micromanipulators.

Advantages: Microinjection is the most precise delivery method, allowing exact control over the amount of material delivered. It is the method of choice for generating transgenic animals, particularly in mouse zygotes for embryo editing.

Disadvantages: Microinjection is extremely labor-intensive and low-throughput—a skilled operator can inject only 100–200 cells per hour. It requires expensive micromanipulation equipment and is not feasible for large-scale experiments.

Other Physical Methods

Sonoporation: Ultrasound waves create transient pores in cell membranes via acoustic cavitation. Microbubbles are often added to enhance the effect. This method is non-invasive and can be applied in vivo, but efficiency is generally lower than electroporation.

Hydrodynamic injection: A large volume of DNA solution (8–10% of body weight) is injected rapidly into the tail vein of a mouse, creating high pressure that forces the solution into hepatocytes. This is used for in vivo liver editing but is not applicable to cell culture.

Biolistic particle delivery (gene gun): DNA- or RNA-coated gold or tungsten microparticles are accelerated into cells using a helium pulse. This is primarily used for plant cells and some hard-to-transfect animal tissues.

Factors Influencing Delivery Efficiency

Cell Type Considerations

Different cell types present distinct barriers to delivery. Suspension cells (e.g., lymphocytes, hematopoietic stem cells) are generally more amenable to electroporation than to lipid-based transfection, which works best on adherent cells. Primary cells are more sensitive to toxicity and often require gentler protocols than immortalized cell lines. The proliferative status matters: plasmid DNA requires nuclear entry during mitosis, so non-dividing cells (e.g., neurons, hepatocytes) are refractory to plasmid transfection but can be edited with mRNA or RNP delivered via electroporation or viral vectors. Cell size also influences electroporation efficiency—larger cells require lower field strengths.

Toxicity and Viability

Every delivery method imposes a toxicity cost. Electroporation causes membrane damage and can trigger apoptosis. Cationic lipids and polymers disrupt membrane integrity and can cause mitochondrial dysfunction. Viral transduction can activate innate immune sensors, leading to interferon responses. The balance between delivery efficiency and cell viability is a central optimization problem. A common approach is to perform a dose-response experiment, testing increasing amounts of delivery reagent or increasing electroporation voltage, and measuring both editing efficiency and viability at each condition.

Off-Target Effects

Off-target editing occurs when Cas9 cleaves genomic sites that are partially homologous to the sgRNA sequence. The duration of Cas9 activity is a major determinant of off-target frequency. Plasmid-based delivery, which produces sustained Cas9 expression, yields the highest off-target rates. RNP delivery, with its short activity window, produces the lowest. Off-target effects can also be influenced by the delivery method itself—electroporation can cause cellular stress that alters DNA repair pathway choice, potentially favoring error-prone NHEJ at off-target sites. For therapeutic applications, minimizing off-target editing is paramount; see CRISPR in Medicine for a discussion of these considerations.

Methods to Evaluate Delivery Success

Confirming that CRISPR components have been delivered and are functional requires multiple complementary assays.

Reporter Assays

Fluorescent reporters: Co-deliver a plasmid encoding green fluorescent protein (GFP) or a fluorescently labeled Cas9 protein. Twenty-four hours post-delivery, assess the percentage of fluorescent cells by flow cytometry. This measures delivery efficiency but not editing efficiency.

Traffic light reporter: A reporter construct contains a GFP gene interrupted by a stop codon and an out-of-frame red fluorescent protein (RFP) gene. Cas9-mediated cleavage at a target site within the construct triggers NHEJ, which can restore the GFP reading frame (indicating indels) or shift the RFP into frame (indicating HDR). This allows simultaneous quantification of NHEJ and HDR by flow cytometry.

Genomic Analysis

T7 endonuclease I (T7EI) assay: PCR-amplify the target region from genomic DNA, denature and re-anneal the amplicons, then digest with T7EI, which cleaves mismatched heteroduplexes. The presence of cleavage products on an agarose gel indicates indels. This assay is semi-quantitative and can estimate editing efficiency by densitometry.

Sanger sequencing with decomposition analysis: PCR-amplify the target locus, perform Sanger sequencing, and analyze the chromatogram with software such as ICE (Inference of CRISPR Edits) or TIDE (Tracking of Indels by Decomposition). These tools quantify the frequency and nature of indels.

Next-generation sequencing (NGS): The gold standard for precise quantification of editing outcomes. NGS provides base-level resolution of indel spectra and can detect off-target edits if targeted amplicon sequencing is performed at predicted off-target sites.

Protein Detection

Western blot: Detect loss of the target protein to confirm functional knockout. This is essential for validating that indels produce a null allele, as some in-frame indels can yield functional proteins.

Immunofluorescence: Stain cells with an antibody against the target protein to assess the proportion of cells that have lost protein expression.

Common Pitfalls and Troubleshooting

Low Efficiency

Symptom: Fewer than 10% of cells show editing.

Possible causes and solutions:

• Poor sgRNA design: Verify that the sgRNA has high on-target activity scores (e.g., using tools like CHOPCHOP or CRISPOR) and that the target site is accessible (open chromatin). Test multiple sgRNAs.
• Insufficient delivery: Increase the amount of CRISPR components, but monitor toxicity. For electroporation, optimize voltage and pulse duration. For lipid transfection, test different reagents—some are optimized for specific cell lines.
• Degraded components: Check RNA integrity by denaturing gel electrophoresis. Store mRNA and sgRNA at −80 °C in RNase-free buffer. Avoid repeated freeze-thaw cycles.
• Cell confluence: Transfect cells at 70–80% confluence. Overly confluent cells take up less material.

High Toxicity

Symptom: More than 50% cell death within 24 hours of delivery.

Possible causes and solutions:

• Excessive electroporation voltage: Reduce voltage by 10–20% and increase pulse duration to compensate.
• High lipid or polymer concentration: Titrate down the delivery reagent. Use a lower dose with a longer incubation time.
• Contaminating endotoxin in plasmid preparations: Purify plasmids using endotoxin-free kits.
• Cas9 protein aggregation: For RNP delivery, ensure the Cas9:sgRNA ratio is correct (1:1.2) and that the complex is formed fresh. Aggregated protein is toxic.

Incorrect Component Ratios

Symptom: Editing works in some experiments but not others, or HDR efficiency is very low.

Possible causes and solutions:

• RNP stoichiometry: The optimal Cas9:sgRNA molar ratio is typically 1:1.2 to 1:3. Excess sgRNA can inhibit editing by competing for Cas9 binding in a non-productive manner.
• mRNA:sgRNA ratio: For mRNA delivery, titrate the sgRNA concentration. Too little sgRNA limits editing; too much can saturate RNA-binding proteins and cause toxicity.
• Donor template for HDR: For HDR experiments, use a single-stranded oligodeoxynucleotide (ssODN) donor at a 100–200-fold molar excess over the RNP. Design homology arms of 40–60 nucleotides on each side of the cut site.

Summary and Best Practices

Choosing a Delivery Method

The choice of delivery method depends on the experimental question, the cell type, and the desired outcome. The table below provides a decision framework.

Key Takeaways

• CRISPR delivery is the critical bottleneck in genome editing; the method determines efficiency, toxicity, and off-target profile.
• The three molecular formats—plasmid DNA, mRNA, and RNP—differ in time to editing, duration of activity, and off-target risk.
• Viral vectors (AAV, lentivirus, adenovirus) offer high efficiency but have cargo size limits, immunogenicity, and integration risks.
• Non-viral chemical methods (LNPs, polymers) are safer but often less efficient, particularly for RNP delivery.
• Physical methods (electroporation, microinjection) provide the most control and are essential for hard-to-transfect cells.
• Always validate delivery success with multiple assays: a reporter for delivery, T7EI or sequencing for editing, and Western blot for protein loss.
• Optimize one variable at a time—delivery reagent dose, cell density, or electroporation parameters—and record viability alongside editing efficiency.

Frequently Asked Questions

How is CRISPR delivered to cells?

CRISPR components are delivered using three broad categories of methods: viral (AAV, lentivirus, adenovirus), non-viral chemical (lipid nanoparticles, cationic polymers), and physical (electroporation, microinjection). The components themselves can be in the form of plasmid DNA, mRNA, or pre-assembled ribonucleoprotein complexes. The choice depends on the cell type, the desired duration of Cas9 expression, and the acceptable level of toxicity.

What is the most common method for CRISPR delivery?

For standard laboratory cell lines, lipid-based transfection of plasmid DNA is the most common method due to its low cost and simplicity. For primary cells and hard-to-transfect cells, electroporation of RNP complexes is the preferred method. In the context of therapeutic applications, lipid nanoparticles delivering mRNA are the leading platform.

Can CRISPR be delivered directly as a protein?

Yes. The Cas9 protein can be produced recombinantly and complexed with a synthetic sgRNA to form a ribonucleoprotein (RNP). The RNP is then delivered into cells, most commonly by electroporation or lipid nanoparticles. This approach provides the fastest onset of editing and the shortest duration of Cas9 activity, minimizing off-target effects.

What are the advantages of viral delivery for CRISPR?

Viral vectors offer high transduction efficiency, the ability to target specific cell types (particularly with AAV serotypes), and the capacity for stable integration (lentivirus) or long-term episomal expression (AAV). They are essential for in vivo delivery and for generating stable cell lines.

Why is CRISPR delivery challenging?

Delivery is challenging because CRISPR components are large, negatively charged molecules that cannot freely cross the plasma membrane. They must survive intracellular nucleases, escape endosomes, and reach the nucleus. Each delivery method has trade-offs between efficiency, toxicity, and cost. Additionally, primary cells and non-dividing cells present specific barriers that require specialized approaches.

What is the difference between transient and stable CRISPR delivery?

Transient delivery (mRNA or RNP) provides a short pulse of Cas9 activity that lasts 24–72 hours, after which the components are degraded. This reduces off-target effects and is suitable for experiments where permanent Cas9 expression is undesirable. Stable delivery (lentiviral integration or plasmid selection) maintains Cas9 expression indefinitely, which is useful for generating cell lines with inducible knockout systems or for long-term screens, but carries a higher off-target risk.

How do I choose a CRISPR delivery method for my experiment?

Consider four factors: (1) the cell type and its amenability to transfection or transduction, (2) the desired duration of Cas9 expression, (3) the acceptable level of toxicity, and (4) the scale of the experiment. For a quick decision: use lipid transfection of plasmid for easy-to-transfect immortalized lines; use electroporation of RNP for primary cells; use lentivirus for stable cell lines; use AAV for in vivo work. Always validate with a pilot experiment before scaling up.

Further Reading

• Salman A et al. Non-Viral Delivery of CRISPR/Cas Cargo to the Retina Using Nanoparticles: Current Possibilities, Challenges, and Limitations. Pharmaceutics. 2022. PubMed 36145593
• Naeem M et al. Stimulus-Responsive Smart Nanoparticles-Based CRISPR-Cas Delivery for Therapeutic Genome Editing. International journal of molecular sciences. 2021. PubMed 34681959
• Sinclair F et al. Recent advances in the delivery and applications of nonviral CRISPR/Cas9 gene editing. Drug delivery and translational research. 2023. PubMed 36988873
• Gori JL et al. Delivery and Specificity of CRISPR-Cas9 Genome Editing Technologies for Human Gene Therapy. Human gene therapy. 2015. PubMed 26068008
• Hamilton JR et al. In vivo human T cell engineering with enveloped delivery vehicles. Nature biotechnology. 2024. PubMed 38212493
• Chang YJ et al. CRISPR Manipulations in Stem Cell Lines. Methods in molecular biology (Clifton, N.J.). 2023. PubMed 36481901

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