The research, led by Sarah Frieda Becker, Marie-Charlotte Morin, Julien Lambert, Shashi Kumar Suman, Francesco Nicola Carelli, Alex Appert, Stéphane Roth, Sarah Hoff-Yoessle, Jessica D. Medina-Sanchez, Manuela Portoso, Julie Ahringer, and Sophie Jarriault, focuses on one of the most remarkable examples of natural cellular plasticity in biology: the conversion of a rectal cell known as the Y cell into a neuron called the PDA. This Y-to-PDA transdifferentiation happens spontaneously during normal worm development, without any injury, experimental reprogramming, or artificial manipulation. Because it occurs reliably and naturally, it offers scientists a clean window into how multicellular organisms permit, control, and restrain changes in cell identity.

For more than a decade, cellular plasticity has been one of the hottest topics in biology. The ability of one cell type to become another underlies both the promise of regenerative medicine and the danger of cancer, where differentiated cells lose their specialized functions and revert to uncontrolled proliferation. Yet while researchers have catalogued many factors that actively push cells toward new identities, the mechanisms that actively prevent such changes, and the ways organisms get around those barriers when change is needed, remain far less well understood. The new study addresses precisely this gap, arguing that the molecular machinery of natural transdifferentiation is more diverse and more layered than previously appreciated.

Using careful genetic analysis in C. elegans, the team showed that lin-15A operates in parallel to plasticity factors that had already been described in the Y-to-PDA conversion. This parallel action is significant. It means that lin-15A is not simply another cog in a known machine but represents a distinct branch of the regulatory network, one that had gone unnoticed because it does not fit the conventional profile of a reprogramming factor. When the researchers examined worms carrying null mutations that eliminate lin-15A function entirely, they found that the transdifferentiation process was compromised, revealing that the gene is required for the natural conversion to unfold properly.

The most striking finding, however, concerns what lin-15A actually does. Rather than acting as an engine that pushes the Y cell toward its neuronal fate, the evidence suggests that LIN-15A works by antagonizing several chromatin-modifying complexes. Chromatin, the packaged form of DNA inside the cell nucleus, is the physical substrate of cell identity. Specialized complexes chemically modify chromatin to lock in the expression patterns that define a differentiated cell, effectively safeguarding that identity against change. These identity safeguarding mechanisms are powerful, and they explain why most cells, even under stress, rarely switch types spontaneously. By interfering with multiple such complexes simultaneously, LIN-15A appears to loosen these locks, lowering the barrier that would otherwise prevent the Y cell from beginning its transformation.

This distinction between driving and licensing is the conceptual heart of the study. The authors propose a two-part model for how controlled cell identity conversions are coordinated in living organisms. In this model, plasticity factors function as Drivers, molecules that actively steer a cell toward its new identity by activating the gene programs of the target cell type. Licensers, by contrast, such as lin-15A, attenuate identity safeguarding mechanisms, clearing the path so that the Drivers can do their work. Neither class alone is sufficient; the conversion requires both the removal of barriers and the provision of directional force. This framework offers a new vocabulary for thinking about natural reprogramming and suggests that similar licensing activities may exist in other transdifferentiation systems across the animal kingdom.

Perhaps the most surprising result is that even cells that are developmentally programmed to undergo transdifferentiation still exhibit reprogramming barriers. One might assume that a cell destined by evolution to change identity would face no resistance at all, that the program would simply run like any other developmental script. The data show otherwise. The Y cell, despite being hardwired for conversion, still needs help overcoming the chromatin-based defenses of its rectal identity. This finding underscores how deeply entrenched cell identity is, and how even nature’s own reprogramming events must actively dismantle protective mechanisms rather than simply switch on new ones.

Equally intriguing is the context-dependence of lin-15A’s role. The study demonstrates that lin-15A is not a core plasticity factor in its own right. It does not universally promote cellular transformations wherever it is expressed. Instead, it functions as a plasticity factor specifically in the Y cell context. This context specificity raises fascinating questions about how licensing activities are targeted to particular cells and particular moments in development. It suggests that the interplay between a gene’s intrinsic biochemical activity and the cellular environment in which it acts determines whether it serves as a general regulator or a highly specialized enabler of change.

The implications extend well beyond worm biology. If natural transdifferentiation relies on a division of labor between Drivers and Licensers, then engineered reprogramming in medicine may need to account for both components. Current approaches to generating replacement cells for regenerative therapies typically focus on delivering powerful driving factors, such as transcription factor cocktails, to force cells into new identities. The new work suggests that a complementary strategy, deliberately weakening the chromatin-based safeguards of the starting cell, could make such conversions more efficient and more faithful to natural processes. Conversely, in cancer, where cells inappropriately shed their differentiated identities, understanding licensing mechanisms could reveal new therapeutic targets: ways to reinforce identity safeguarding and prevent malignant dedifferentiation.

The study also highlights the enduring value of C. elegans as a model for fundamental discovery. Because the worm’s cells can be followed individually through development, and because the Y-to-PDA conversion is a natural event that can be observed and genetically dissected with precision, researchers can identify mechanisms that would be nearly impossible to isolate in more complex systems. The identification of a THAP domain gene as a licensing factor adds a new family of proteins to the plasticity toolbox and opens avenues for exploring whether related genes perform analogous roles in other organisms, including humans. As the authors conclude, diverse molecular activities coordinate controlled cell identity conversions, and recognizing that some of these activities work by removing barriers rather than providing direction may fundamentally change how scientists approach the problem of cellular identity, both in the laboratory and, eventually, at the bedside.

Subject of Research: The role of the lin-15A gene in licensing natural Y-to-PDA transdifferentiation in C. elegans by antagonizing chromatin-based identity safeguarding mechanisms

Article Title: The SynMuvA lin-15A licenses natural transdifferentiation by antagonizing identity safeguarding mechanisms

Article References: Becker, S. F., Morin, M.-C., Lambert, J., Suman, S. K., Carelli, F. N., Appert, A., Roth, S., Hoff-Yoessle, S., Medina-Sanchez, J. D., Portoso, M., Ahringer, J., & Jarriault, S. (2026). The SynMuvA lin-15A licenses natural transdifferentiation by antagonizing identity safeguarding mechanisms. PLOS Genetics, 22(9), e1012290. https://doi.org/10.1371/journal.pgen.1012290

Image Credits: AI Generated

DOI: 10.1371/journal.pgen.1012290

Keywords: cell plasticity, transdifferentiation, lin-15A, Caenorhabditis elegans, chromatin, cell identity, PLOS Genetics, reprogramming, THAP domain, developmental biology, gene regulation, regenerative medicine

The resource, described by Laura Scheinfeldt and colleagues, consists of five induced pluripotent stem cell lines derived from apparently healthy donors, each paired with its matched parental cell line. All of the biospecimens are being made available to the scientific community through the National Institute of General Medical Sciences Human Genetic Cell Repository, which is housed at Coriell in Camden, New Jersey. Crucially, the cell lines are accompanied by publicly available high-fidelity, or HiFi, whole-genome sequencing data, along with a suite of web-based search tools that allow any researcher to visualize and explore the genetic variants found in each line.

The choice of sequencing technology matters enormously here. Traditional short-read sequencing, which breaks DNA into fragments of a few hundred base pairs and reassembles them by matching them to a reference genome, is excellent at detecting single nucleotide variants, the single-letter changes in DNA that are the most common form of human genetic variation. But it struggles with structural variants, which include deletions, duplications, inversions, and insertions that can span thousands or even millions of base pairs. These large rearrangements are notoriously difficult to resolve with short reads because the broken pieces of DNA often do not map cleanly to the reference. Long-read sequencing, by contrast, reads individual DNA molecules that stretch tens of thousands of base pairs, allowing structural variants to be observed directly rather than inferred.

HiFi sequencing, the specific long-read approach used in this study, adds another layer of quality. It produces long reads with very high per-base accuracy, combining the reach of long-read technology with the precision traditionally associated with short reads. For a resource intended to serve as a reference standard for the community, that combination is essential. Researchers who download these cell lines and their sequencing data can be confident that the structural variant calls, in particular, reflect genuine features of the genome rather than artifacts of the assembly process.

To assess how well each iPSC line preserved its donor’s genome, the team compared the variants detected in each iPSC line with those in its matched parental cell line. The logic is straightforward: reprogramming should, in principle, leave the genome untouched, so any difference between an iPSC and its parent could signal a change introduced during reprogramming or subsequent cell culture. The results were encouraging overall. Concordance between iPSC lines and their parental counterparts was generally high for both structural variants and single nucleotide variants, suggesting that the reprogramming methods used for most of the lines preserved genomic integrity well.

There was, however, one notable exception, and it carries a cautionary message for the field. One of the five iPSC lines, which had been reprogrammed using a retroviral method, showed a reduction in concordance with its parental cell line. The authors note that this finding is consistent with previously reported concerns about retroviral reprogramming. Retroviruses integrate into the host genome to deliver the reprogramming factors, an approach that has been associated in earlier studies with genomic disruption and with the introduction of copy number changes. While the study does not claim that retroviral reprogramming is inherently unsafe, the observation reinforces a growing consensus that the reprogramming method itself can leave a measurable genomic footprint, and that newer, integration-free methods may better preserve the original genome.

Beyond the concordance analysis, the resource includes annotations that greatly expand its practical usefulness. Each line has been characterized for pharmacogenomic variants, the genetic differences that influence how individuals respond to drugs, and for human leukocyte antigen, or HLA, genes, which encode the proteins that the immune system uses to distinguish self from non-self. HLA typing is critical for any application involving immune compatibility, including potential cell therapies and the development of isogenic controls in immunological experiments. Pharmacogenomic annotation, meanwhile, makes these lines immediately relevant to research on variable drug response, an area where in vitro models derived from well-characterized donors can reveal why the same medication works well for one patient and poorly for another.

The web-based search tools accompanying the resource deserve particular attention because they address a chronic bottleneck in genomics: accessibility of data. Whole-genome sequencing datasets are often deposited in repositories in formats that require substantial computational expertise to parse. By building user-friendly interfaces for visualizing and exploring the structural and single nucleotide variants in these lines, the Coriell team has lowered the barrier for laboratory scientists who may not be bioinformaticians but who need to know, for example, whether a candidate gene in their study carries an interesting variant in one of the available lines. The authors acknowledge the critical contributions of Phillip Hodges to the design, development, and ongoing support of the information technology infrastructure behind these tools, and Jozef Madzo for advice on the genomic data collection.

The samples themselves come from an unusual and forward-looking source. All biospecimens were donated by participants in the Personal Genome Project, an initiative in which volunteers consent to have their biospecimens and associated genomic data used for general research purposes. This open-consent framework means that researchers using these lines can access genomic information that is directly tied to the donor, rather than working with anonymized samples whose genetic data cannot be shared. The repository collection is approved by the Coriell Institutional Review Board, and the participants’ consent covers broad research use, which maximizes the flexibility of the resource for future, unforeseen applications.

The broader significance of this work lies in what it offers to the reproducibility crisis in biomedical research. Cell-based experiments are notoriously sensitive to the identity and quality of the cell lines used, and misidentified or poorly characterized lines have undermined countless studies over the decades. By pairing renewable iPSC lines with matched parental cells, high-quality long-read genome sequences, pharmacogenomic and HLA annotations, and accessible search tools, this resource provides a level of characterization that individual laboratories would find difficult and expensive to replicate on their own. The funding came from the National Institute of General Medical Sciences and the National Human Genome Research Institute, reflecting the federal investment in shared biomedical infrastructure. For researchers interested in the cell-type-specific functional effects of genetic, genomic, and pharmacogenomic variation, the message of the study is clear: a rigorously characterized, openly available set of in vitro models now exists, and it is designed to make the resulting science both higher in quality and easier to reproduce.

Subject of Research: A long-read whole-genome sequencing characterization of induced pluripotent stem cell lines and matched parental cells for enhanced in vitro disease modeling

Article Title: New iPSC resource with long-read whole genome sequencing characterizations for enhanced in vitro modeling

Article References: Scheinfeldt, L., Pompetti, A., Calendo, G., Pozner, T., Grandizio, C., Smith, G., Hodges, K., Gharani, N., Kusic, D., Mitchell, M., & Turan, N. (2026). New iPSC resource with long-read whole genome sequencing characterizations for enhanced in vitro modeling. BMC Genomics. https://doi.org/10.1186/s12864-026-13303-8

Image Credits: AI Generated

DOI: 10.1186/s12864-026-13303-8

Keywords: iPSC, long-read sequencing, HiFi whole-genome sequencing, structural variants, single nucleotide variants, pharmacogenomics, HLA genes, biorepository, reprogramming, in vitro modeling, genomic concordance, Coriell Institute

The two proteins in question are PARK7, also known as DJ-1, and PINK1. Both are best known to the public through their connection to familial Parkinson’s disease, where loss-of-function mutations sensitize neurons to oxidative damage and mitochondrial dysfunction. In the new work, the Tsukuba team asked whether these same proteins do something entirely different in a very different cellular context: the dramatic transformation that occurs when mouse embryonic fibroblasts are pushed toward pluripotency by reprogramming factors. PARK7 is a multifunctional, redox-sensitive protein long implicated in buffering oxidative stress and modulating transcription, and earlier reports had suggested it could associate with the promoter of Nanog, a master gene of pluripotency, and even suppress reprogramming efficiency. That hint of an inhibitory role made PARK7 an intriguing suspect.

To test the idea, the researchers depleted Park7 in mouse embryonic fibroblasts undergoing reprogramming and monitored the emergence of Nanog-positive colonies, a standard readout of successful pluripotency induction. The result was striking: knocking down Park7 enhanced colony formation, with the effect most pronounced during the early phases of reprogramming. In other words, removing PARK7 made it easier for somatic cells to cross the initial barriers on the road to pluripotency. This positioned PARK7 not as a passive bystander but as an active regulator of the process, and it raised the obvious question of how a protein best known for antioxidant defense could, when removed, actually improve the efficiency of cellular rejuvenation.

The answer, it turns out, lies in reactive oxygen species. Reprogramming is metabolically traumatic: a cell that has spent its life burning glucose efficiently through mitochondrial oxidative phosphorylation must tear down and rebuild its entire energy economy, ultimately adopting the glycolytic, lactate-producing metabolism characteristic of embryonic stem cells. That transition is accompanied by bursts of reactive oxygen species, which at controlled levels act as signaling molecules that help drive the switch. Using paused iPSCs, a valuable experimental system in which cells are held in a partially reprogrammed state and can be interrogated in detail, the team showed that depleting Park7 increased both mitochondrial and cytosolic ROS, stabilized HIF-1α, the hypoxia-inducible transcription factor that commands the glycolytic program, promoted the expression of glycolytic genes, and upregulated pluripotency markers.

The causal chain became clear when the researchers added antioxidants to the culture. Antioxidant treatment substantially blunted all of these effects, indicating that the enhanced reprogramming phenotype seen upon Park7 loss was driven by ROS-mediated metabolic remodeling rather than by some unrelated function of the protein. In essence, PARK7 normally keeps a brake on ROS levels, and that brake, paradoxically, restrains the very oxidative signals that help push a cell toward pluripotency. When the brake is released, ROS rise, HIF-1α accumulates, glycolysis genes switch on, and the cell slides more readily into its new pluripotent identity. It is a vivid demonstration that in reprogramming, a little oxidative stress is not the enemy but an ally.

The study also uncovered a second, compensatory layer of redox regulation. The elevated ROS triggered by Park7 depletion activated NRF2, the master transcription factor of antioxidant defense, switching on NRF2-dependent antioxidant transcriptional programs. This reveals a built-in feedback loop: as ROS climb and drive metabolic remodeling, the cell simultaneously mounts a protective antioxidant response, presumably to keep the oxidative surge within tolerable limits. The interplay between these pro-signaling and protective arms of the redox system highlights how finely balanced the reprogramming environment must be, and it suggests that manipulating this balance could be a way to tune reprogramming efficiency in the laboratory.

Perhaps the most consequential discovery, however, concerns PINK1. The team found that Park7 depletion reduces the expression of Pink1, and that knocking down Pink1 phenocopies the loss of Park7, producing the same ROS elevation, metabolic shift, and pluripotency marker upregulation. Most tellingly, restoring wild-type PINK1 reversed the increase in pluripotency markers caused by Park7 loss. Together, these experiments establish PINK1 as the essential downstream mediator of PARK7 in this cascade. The two Parkinson’s-linked proteins, it appears, operate as a functional axis: PARK7 upstream, sustaining PINK1 expression, and PINK1 downstream, executing the ROS-suppressing and metabolic functions that keep reprogramming in check.

This PARK7–PINK1 axis is more than a curiosity of stem cell biology. It suggests that the same molecular machinery whose failure contributes to neurodegeneration also serves as a gatekeeper during the acquisition of pluripotency, coordinating three intertwined processes: suppression of reactive oxygen species, glycolytic metabolic remodeling, and the expression of pluripotency genes. For researchers trying to generate iPSCs more efficiently and more safely, the findings point to concrete levers. Modulating PARK7 or PINK1 activity, or carefully titrating ROS with antioxidants, could in principle shift cells along the reprogramming trajectory. At the same time, the work cautions that redox manipulation is a double-edged sword, since the NRF2 response shows the cell actively defending itself against the very signals that promote its transformation.

There are also broader implications for understanding disease. PARK7 and PINK1 are central figures in the mitochondrial quality control literature, and this study ties them to HIF-1α-driven metabolic switching and NRF2-mediated antioxidant transcription, linking several of the most important stress-response pathways in cell biology into a single regulatory circuit. Whether the axis operates similarly in human cells, and whether it influences the quality and genomic stability of the resulting iPSCs, are questions the field will now want to pursue. The experiments were conducted in mouse embryonic fibroblasts and paused iPSCs, so translating the mechanism to human reprogramming systems will be an essential next step.

What the study delivers today is a mechanistic framework with immediate experimental value. By showing that PARK7 restrains reprogramming primarily through PINK1-dependent control of ROS, the Tsukuba team has converted a long-standing puzzle about DJ-1’s role at the Nanog promoter into a coherent signaling pathway that connects redox balance, metabolism, and gene expression during one of biology’s most dramatic cellular transformations. As regenerative medicine moves closer to the clinic, understanding such gatekeepers, and learning when to release them and when to respect them, may prove as important as the reprogramming factors themselves. The full open-access study is available in Cellular and Molecular Life Sciences for readers who wish to explore the experimental details.

Subject of Research: The role of the PARK7–PINK1 axis in redox balance and metabolic remodeling during induced pluripotent stem cell reprogramming

Article Title: A PARK7–PINK1 axis coordinates redox balance and metabolic remodeling during somatic cell reprogramming

Article References: Mensah, E. O., Burramsetty, A. K., Kamata, H., Jiang, Z., Fukuda, A., Hisatake, K., & Nishimura, K. (2026). A PARK7–PINK1 axis coordinates redox balance and metabolic remodeling during somatic cell reprogramming. Cellular and Molecular Life Sciences. https://doi.org/10.1007/s00018-026-06468-8

Image Credits: AI Generated

DOI: 10.1007/s00018-026-06468-8

Keywords: PARK7, DJ-1, PINK1, iPSCs, reprogramming, pluripotency, reactive oxygen species, HIF-1α, NRF2, metabolic remodeling, redox biology, mitochondria

The core innovation is deceptively simple. Rather than relying on invasive skin biopsies, blood draws or urine collection, the protocol uses hairs plucked with intact follicles, ideally in the anagen or growth phase, when the follicle is rich in proliferative keratinocytes. Once plucked, the hairs are placed in a kit and can be mailed over long distances without refrigeration. In the laboratory, keratinocytes are released from the follicles by trypsinization, an enzymatic digestion that separates the cells from the hair shaft, and are then cultured under conditions that preserve their proliferative capacity. The authors report that samples remain stable for days at ambient temperature, provided standard biosafety precautions are observed, which makes ordinary postal and courier services viable conduits for human biological material.

Why does the choice of starting cell matter so much? Induced pluripotent stem cells, first generated by Shinya Yamanaka and colleagues in 2007 through the forced expression of defined transcription factors, can differentiate into all three embryonic lineages, including the neural lineage that gives rise to neurons and glia. But the quality and efficiency of reprogramming depend heavily on the source cell. Dermal fibroblasts require a punch biopsy, an uncomfortable procedure that typically must be performed by a clinician. Peripheral blood mononuclear cells require venipuncture and careful handling, and although blood held at room temperature has been used successfully, the window is limited. Renal epithelial cells from urine are noninvasive but yield variable numbers of cells and are not suitable for every donor. Keratinocytes, by contrast, reprogram efficiently, and hair plucking is essentially painless.

The Yale team’s protocol lowers the technical barrier even further by requiring fewer follicles than previous hair-based approaches. Earlier methods for isolating keratinocytes from plucked hair existed, including protocols published by Aasen and colleagues in 2008 and 2010, but they generally demanded either fresh local collection or specialized handling. The new kit-based workflow explicitly anticipates the realities of remote participation: a donor, a family member or a healthcare provider can perform the collection after watching a short instructional video that accompanies the protocol, and the resulting sample tolerates the delays of long-distance shipping. This matters enormously for rare disease research, where patients are geographically dispersed and where systematic reviews have documented substantial inequities in access to clinical genetic services.

Once the keratinocytes arrive in the laboratory, the workflow follows a well-trodden but carefully optimized path. The cells are expanded in culture, with the Rho kinase inhibitor Y-27632 playing a supporting role in improving survival, a trick borrowed from the keratinocyte literature where ROCK inhibition prolongs the lifespan of adult cells in vitro. Reprogramming then converts the keratinocytes into iPS cells, a process the protocol completes within roughly two months of receiving the hair samples. Notably, the authors emphasize that the procedure requires only basic familiarity with mammalian cell culture techniques and no specialized equipment beyond what a standard cell biology laboratory already possesses. That accessibility is a deliberate design choice: the protocol is written to be executable by labs that have never worked with human iPS cells before.

Quality control is built into the workflow. The published protocol includes characterization steps confirming that the resulting iPS cells express canonical pluripotency markers, retain a normal karyotype, and can differentiate into all three germ layers, including neural lineages. The authors demonstrate the full pipeline by generating cerebral organoids, three-dimensional self-organizing cultures that recapitulate key features of early human brain development. Organoid generation from the iPS cells takes 30 to 40 days and requires one piece of specialized equipment, an orbital shaker, which keeps the growing organoids suspended and nourished in culture. Whole-mount imaging and immunostaining confirm that the organoids contain the expected neural cell populations, establishing that hair-derived iPS cells are fully competent for demanding three-dimensional differentiation protocols.

The protocol did not emerge in a vacuum. It was developed and refined in the course of a primary research study, published in Nature in 2025, in which Zhang and colleagues showed that dysregulation of mTOR signalling is a converging mechanism in lissencephaly, a severe malformation of cortical development. For that study, the team needed iPS cells and brain organoids from patients with rare neurogenetic conditions, many of whom lived far from any research center. The kit-based hair collection method proved to be the practical answer, and the new Nature Protocols article distills that hard-won experience into a form other laboratories can adopt directly. The authors acknowledge the patients and families who contributed samples, underscoring that the method was shaped by the needs of the very people it is meant to serve.

The broader implications reach into drug development, disease modeling and eventually cell therapy. Human iPS cell-derived models allow researchers to study cellular and molecular mechanisms of disease in genuinely human tissue, something animal models often fail to capture, and cerebral organoids in particular have transformed the study of neurodevelopmental disorders since Lancaster and colleagues first described them in 2013. By making the front end of that pipeline, patient sample acquisition, dramatically easier, the Yale protocol could expand the diversity of genetic backgrounds represented in organoid studies, a long-standing concern in a field where most cell lines derive from patients already connected to major academic medical centers. Populations in low-resource settings, pediatric patients for whom blood draws are difficult, and elderly donors with fragile veins all stand to benefit from a collection method that requires nothing more than a pair of tweezers and a mailing envelope.

There are, of course, practical considerations. The protocol specifies that hairs must be plucked with follicles intact, since the follicle bulb contains the keratinocyte population of interest, and the accompanying video walks collectors through identifying suitable anagen-phase hairs. Shipping times must remain within the window during which the keratinocytes stay viable at ambient temperature, and laboratories must handle all human material under appropriate biosafety procedures. Reprogramming efficiency, while generally high for keratinocytes, still varies between donors, as it does for all somatic cell sources. Yet the authors argue that the advantages outweigh these constraints: the method is noninvasive, the samples are robust, the timeline is competitive, and the equipment requirements are minimal. As personalized medicine pushes toward models built from each patient’s own genome, protocols like this one may determine who gets to participate. A technology that turns a handful of plucked hairs into a patient-specific mini brain, mailed across continents in an ordinary package, is a striking reminder that sometimes the most transformative tools in biomedicine are also the most humble.

Subject of Research: A kit-based protocol for remote collection of hair follicle keratinocytes and their reprogramming into induced pluripotent stem cells for cerebral organoid generation

Article Title: Kit-based remote collection and isolation of human reprogrammable somatic cells for generation of induced pluripotent stem cells and cerebral organoids

Article References: Cheng, I. Q., Ruiz, J. F., Casalino, E. K., Zhang, C., & Louvi, A. (2026). Kit-based remote collection and isolation of human reprogrammable somatic cells for generation of induced pluripotent stem cells and cerebral organoids. Nature Protocols. https://doi.org/10.1038/s41596-026-01440-z

Image Credits: AI Generated

DOI: 10.1038/s41596-026-01440-z

Keywords: induced pluripotent stem cells, keratinocytes, hair follicles, cerebral organoids, reprogramming, remote sample collection, disease modeling, personalized medicine, neurodevelopmental disorders, Nature Protocols, cell culture, lissencephaly