what does it mean for a cell to differentiate
Stalk cell differentiation into diverse tissue types.
Cell-count distribution featuring cellular differentiation for three types of cells (progenitor , osteoblast , and chondrocyte ) exposed to pro-osteoblast stimulus.[1]
Cellular differentiation is the process in which a stem cell alters from 1 type to a differentiated one[ii] [3] Usually, the jail cell changes to a more specialized blazon. Differentiation happens multiple times during the development of a multicellular organism as it changes from a uncomplicated zygote to a complex system of tissues and prison cell types. Differentiation continues in machismo as developed stem cells divide and create fully differentiated daughter cells during tissue repair and during normal cell turnover. Some differentiation occurs in response to antigen exposure. Differentiation dramatically changes a jail cell's size, shape, membrane potential, metabolic activity, and responsiveness to signals. These changes are largely due to highly controlled modifications in cistron expression and are the report of epigenetics. With a few exceptions, cellular differentiation near never involves a modify in the DNA sequence itself. Although metabolic composition does go altered quite dramatically[4] where stem cells are characterized by abundant metabolites with highly unsaturated structures whose levels decrease upon differentiation. Thus, different cells can have very different physical characteristics despite having the same genome.
A specialized type of differentiation, known as terminal differentiation, is of importance in some tissues, for example vertebrate nervous arrangement, striated muscle, epidermis and gut. During last differentiation, a precursor cell formerly capable of cell division, permanently leaves the cell cycle, dismantles the cell cycle machinery and oft expresses a range of genes characteristic of the cell's last function (eastward.g. myosin and actin for a muscle prison cell). Differentiation may continue to occur after terminal differentiation if the capacity and functions of the prison cell undergo farther changes.
Amidst dividing cells, in that location are multiple levels of prison cell potency, the cell'due south ability to differentiate into other cell types. A greater potency indicates a larger number of jail cell types that can be derived. A prison cell that can differentiate into all jail cell types, including the placental tissue, is known as totipotent. In mammals, only the zygote and subsequent blastomeres are totipotent, while in plants, many differentiated cells can become totipotent with simple laboratory techniques. A cell that can differentiate into all cell types of the adult organism is known as pluripotent. Such cells are called meristematic cells in higher plants and embryonic stem cells in animals, though some groups written report the presence of adult pluripotent cells. Virally induced expression of iv transcription factors Oct4, Sox2, c-Myc, and Klf4 (Yamanaka factors) is sufficient to create pluripotent (iPS) cells from developed fibroblasts.[5] A multipotent cell is one that can differentiate into multiple different, but closely related cell types.[six] Oligopotent cells are more restricted than multipotent, but can all the same differentiate into a few closely related cell types.[6] Finally, unipotent cells can differentiate into only one jail cell type, but are capable of cocky-renewal.[half dozen] In cytopathology, the level of cellular differentiation is used as a measure of cancer progression. "Class" is a marker of how differentiated a prison cell in a tumor is.[7]
Mammalian cell types [edit]
3 basic categories of cells brand up the mammalian torso: germ cells, somatic cells, and stem cells. Each of the approximately 37.2 trillion (3.72x1013) cells in an adult human has its own copy or copies of the genome except certain cell types, such as red claret cells, that lack nuclei in their fully differentiated state. Virtually cells are diploid; they have two copies of each chromosome. Such cells, called somatic cells, brand upward well-nigh of the human trunk, such as pare and muscle cells. Cells differentiate to specialize for unlike functions.[8]
Germ line cells are whatever line of cells that give rise to gametes—eggs and sperm—and thus are continuous through the generations. Stalk cells, on the other manus, have the ability to dissever for indefinite periods and to give ascension to specialized cells. They are best described in the context of normal human development.[ commendation needed ]
Development begins when a sperm fertilizes an egg and creates a unmarried cell that has the potential to form an entire organism. In the first hours after fertilization, this cell divides into identical cells. In humans, approximately four days after fertilization and after several cycles of cell division, these cells begin to specialize, forming a hollow sphere of cells, called a blastocyst.[nine] The blastocyst has an outer layer of cells, and inside this hollow sphere, at that place is a cluster of cells called the inner prison cell mass. The cells of the inner prison cell mass go along to form nigh all of the tissues of the homo body. Although the cells of the inner cell mass can form virtually every type of cell establish in the human being body, they cannot grade an organism. These cells are referred to equally pluripotent.[x]
Pluripotent stalk cells undergo further specialization into multipotent progenitor cells that then requite rise to functional cells. Examples of stem and progenitor cells include:[ citation needed ]
- Radial glial cells (embryonic neural stem cells) that give rising to excitatory neurons in the fetal brain through the procedure of neurogenesis.[eleven] [12] [13]
- Hematopoietic stem cells (developed stalk cells) from the bone marrow that give rising to red claret cells, white blood cells, and platelets
- Mesenchymal stalk cells (adult stalk cells) from the bone marrow that give rise to stromal cells, fat cells, and types of bone cells
- Epithelial stem cells (progenitor cells) that give rise to the various types of skin cells
- Muscle satellite cells (progenitor cells) that contribute to differentiated muscle tissue.
A pathway that is guided past the prison cell adhesion molecules consisting of four amino acids, arginine, glycine, asparagine, and serine, is created as the cellular blastomere differentiates from the single-layered blastula to the three primary layers of germ cells in mammals, namely the ectoderm, mesoderm and endoderm (listed from nearly distal (exterior) to proximal (interior)). The ectoderm ends upwards forming the skin and the nervous system, the mesoderm forms the bones and muscular tissue, and the endoderm forms the internal organ tissues.
Dedifferentiation [edit]
Micrograph of a liposarcoma with some dedifferentiation, that is not identifiable every bit a liposarcoma, (left edge of image) and a differentiated component (with lipoblasts and increased vascularity (correct of prototype)). Fully differentiated (morphologically benign) adipose tissue (heart of the image) has few blood vessels. H&E stain.
Dedifferentiation, or integration, is a cellular procedure ofttimes seen in more basal life forms such as worms and amphibians in which a partially or terminally differentiated prison cell reverts to an before developmental phase, usually as part of a regenerative process.[fourteen] [xv] Dedifferentiation also occurs in plants.[16] Cells in cell culture can lose properties they originally had, such equally protein expression, or change shape. This process is also termed dedifferentiation.[17]
Some believe dedifferentiation is an aberration of the normal development wheel that results in cancer,[18] whereas others believe information technology to be a natural part of the immune response lost by humans at some point as a result of evolution.
A pocket-size molecule dubbed reversine, a purine analog, has been discovered that has proven to induce dedifferentiation in myotubes. These dedifferentiated cells could then redifferentiate into osteoblasts and adipocytes.[19]
Diagram exposing several methods used to revert developed somatic cells to totipotency or pluripotency.
Mechanisms [edit]
Mechanisms of cellular differentiation.
Each specialized cell type in an organism expresses a subset of all the genes that constitute the genome of that species. Each cell type is defined past its detail pattern of regulated gene expression. Prison cell differentiation is thus a transition of a prison cell from i cell blazon to another and it involves a switch from one design of gene expression to some other. Cellular differentiation during development tin be understood as the result of a factor regulatory network. A regulatory gene and its cis-regulatory modules are nodes in a gene regulatory network; they receive input and create output elsewhere in the network.[xx] The systems biology arroyo to developmental biology emphasizes the importance of investigating how developmental mechanisms interact to produce anticipated patterns (morphogenesis). All the same, an culling view has been proposed recently[ when? ] [ by whom? ]. Based on stochastic gene expression, cellular differentiation is the result of a Darwinian selective process occurring among cells. In this frame, protein and factor networks are the event of cellular processes and non their cause.[ citation needed ]
An overview of major signal transduction pathways.
While evolutionarily conserved molecular processes are involved in the cellular mechanisms underlying these switches, in animal species these are very different from the well-characterized factor regulatory mechanisms of leaner, and even from those of the animals' closest unicellular relatives.[21] Specifically, cell differentiation in animals is highly dependent on biomolecular condensates of regulatory proteins and enhancer DNA sequences.
Cellular differentiation is frequently controlled by cell signaling. Many of the indicate molecules that convey data from prison cell to cell during the control of cellular differentiation are called growth factors. Although the details of specific indicate transduction pathways vary, these pathways often share the following general steps. A ligand produced past i cell binds to a receptor in the extracellular region of some other jail cell, inducing a conformational alter in the receptor. The shape of the cytoplasmic domain of the receptor changes, and the receptor acquires enzymatic activity. The receptor so catalyzes reactions that phosphorylate other proteins, activating them. A pour of phosphorylation reactions somewhen activates a dormant transcription cistron or cytoskeletal protein, thus contributing to the differentiation process in the target cell.[22] Cells and tissues can vary in competence, their ability to respond to external signals.[23]
Signal consecration refers to cascades of signaling events, during which a cell or tissue signals to another cell or tissue to influence its developmental fate.[23] Yamamoto and Jeffery[24] investigated the role of the lens in center formation in cave- and surface-habitation fish, a striking example of induction.[23] Through reciprocal transplants, Yamamoto and Jeffery[24] plant that the lens vesicle of surface fish can induce other parts of the eye to develop in cavern- and surface-habitation fish, while the lens vesicle of the cave-dwelling fish cannot.[23]
Other important mechanisms fall under the category of asymmetric jail cell divisions, divisions that give ascension to daughter cells with singled-out developmental fates. Disproportionate cell divisions can occur because of asymmetrically expressed maternal cytoplasmic determinants or because of signaling.[23] In the quondam mechanism, distinct daughter cells are created during cytokinesis considering of an uneven distribution of regulatory molecules in the parent cell; the distinct cytoplasm that each daughter prison cell inherits results in a distinct design of differentiation for each daughter jail cell. A well-studied example of pattern formation by asymmetric divisions is torso axis patterning in Drosophila. RNA molecules are an important type of intracellular differentiation command point. The molecular and genetic basis of disproportionate prison cell divisions has also been studied in greenish algae of the genus Volvox, a model system for studying how unicellular organisms can evolve into multicellular organisms.[23] In Volvox carteri, the xvi cells in the anterior hemisphere of a 32-cell embryo divide asymmetrically, each producing one big and ane pocket-size daughter cell. The size of the cell at the end of all jail cell divisions determines whether it becomes a specialized germ or somatic cell.[23] [25]
Epigenetic control [edit]
Since each cell, regardless of cell blazon, possesses the same genome, determination of prison cell type must occur at the level of gene expression. While the regulation of cistron expression tin occur through cis- and trans-regulatory elements including a gene's promoter and enhancers, the problem arises every bit to how this expression blueprint is maintained over numerous generations of prison cell sectionalisation. Every bit information technology turns out, epigenetic processes play a crucial role in regulating the decision to adopt a stem, progenitor, or mature jail cell fate. This section volition focus primarily on mammalian stem cells.
In systems biology and mathematical modeling of factor regulatory networks, jail cell-fate determination is predicted to exhibit certain dynamics, such as attractor-convergence (the attractor tin can be an equilibrium point, limit wheel or strange attractor) or oscillatory.[26]
Importance of epigenetic control [edit]
The first question that tin be asked is the extent and complexity of the function of epigenetic processes in the determination of cell fate. A clear respond to this question can be seen in the 2011 paper by Lister R, et al. [27] on abnormal epigenomic programming in human being induced pluripotent stem cells. As induced pluripotent stalk cells (iPSCs) are thought to mimic embryonic stalk cells in their pluripotent properties, few epigenetic differences should exist between them. To test this prediction, the authors conducted whole-genome profiling of Deoxyribonucleic acid methylation patterns in several human embryonic stem jail cell (ESC), iPSC, and progenitor cell lines.
Female adipose cells, lung fibroblasts, and foreskin fibroblasts were reprogrammed into induced pluripotent state with the OCT4, SOX2, KLF4, and MYC genes. Patterns of DNA methylation in ESCs, iPSCs, somatic cells were compared. Lister R, et al. observed pregnant resemblance in methylation levels between embryonic and induced pluripotent cells. Around 80% of CG dinucleotides in ESCs and iPSCs were methylated, the same was true of only lx% of CG dinucleotides in somatic cells. In addition, somatic cells possessed minimal levels of cytosine methylation in non-CG dinucleotides, while induced pluripotent cells possessed similar levels of methylation as embryonic stalk cells, betwixt 0.5 and 1.v%. Thus, consistent with their respective transcriptional activities,[27] DNA methylation patterns, at to the lowest degree on the genomic level, are similar betwixt ESCs and iPSCs.
However, upon examining methylation patterns more closely, the authors discovered 1175 regions of differential CG dinucleotide methylation between at to the lowest degree i ES or iPS cell line. Past comparing these regions of differential methylation with regions of cytosine methylation in the original somatic cells, 44-49% of differentially methylated regions reflected methylation patterns of the respective progenitor somatic cells, while 51-56% of these regions were dissimilar to both the progenitor and embryonic prison cell lines. In vitro-induced differentiation of iPSC lines saw transmission of 88% and 46% of hyper and hypo-methylated differentially methylated regions, respectively.
Two conclusions are readily credible from this study. First, epigenetic processes are heavily involved in prison cell fate determination, as seen from the similar levels of cytosine methylation betwixt induced pluripotent and embryonic stem cells, consistent with their respective patterns of transcription. 2nd, the mechanisms of reprogramming (and by extension, differentiation) are very complex and cannot exist easily duplicated, as seen by the pregnant number of differentially methylated regions between ES and iPS jail cell lines. At present that these two points have been established, we tin examine some of the epigenetic mechanisms that are thought to regulate cellular differentiation.
Mechanisms of epigenetic regulation [edit]
Pioneer factors (Oct4, Sox2, Nanog) [edit]
Three transcription factors, OCT4, SOX2, and NANOG – the start two of which are used in induced pluripotent stem cell (iPSC) reprogramming, along with Klf4 and c-Myc – are highly expressed in undifferentiated embryonic stem cells and are necessary for the maintenance of their pluripotency.[28] It is idea that they achieve this through alterations in chromatin structure, such as histone modification and DNA methylation, to restrict or let the transcription of target genes. While highly expressed, their levels crave a precise balance to maintain pluripotency, perturbation of which will promote differentiation towards different lineages based on how the gene expression levels alter. Differential regulation of October-4 and SOX2 levels accept been shown to precede germ layer fate pick.[29] Increased levels of Oct4 and decreased levels of Sox2 promote a mesendodermal fate, with Oct4 actively suppressing genes associated with a neural ectodermal fate. Similarly, Increased levels of Sox2 and decreased levels of Oct4 promote differentiation towards a neural ectodermal fate, with Sox2 inhibiting differentiation towards a mesendodermal fate. Regardless of the lineage cells differentiate down, suppression of NANOG has been identified as a necessary prerequisite for differentiation.[29]
Polycomb repressive circuitous (PRC2) [edit]
In the realm of cistron silencing, Polycomb repressive circuitous ii, one of two classes of the Polycomb grouping (PcG) family of proteins, catalyzes the di- and tri-methylation of histone H3 lysine 27 (H3K27me2/me3).[28] [30] [31] By binding to the H3K27me2/3-tagged nucleosome, PRC1 (also a circuitous of PcG family proteins) catalyzes the mono-ubiquitinylation of histone H2A at lysine 119 (H2AK119Ub1), blocking RNA polymerase II action and resulting in transcriptional suppression.[28] PcG knockout ES cells exercise non differentiate efficiently into the 3 germ layers, and deletion of the PRC1 and PRC2 genes leads to increased expression of lineage-affiliated genes and unscheduled differentiation.[28] Presumably, PcG complexes are responsible for transcriptionally repressing differentiation and development-promoting genes.
Trithorax grouping proteins (TrxG) [edit]
Alternately, upon receiving differentiation signals, PcG proteins are recruited to promoters of pluripotency transcription factors. PcG-deficient ES cells can begin differentiation but cannot maintain the differentiated phenotype.[28] Simultaneously, differentiation and development-promoting genes are activated past Trithorax group (TrxG) chromatin regulators and lose their repression.[28] [31] TrxG proteins are recruited at regions of high transcriptional activity, where they catalyze the trimethylation of histone H3 lysine iv (H3K4me3) and promote factor activation through histone acetylation.[31] PcG and TrxG complexes engage in direct competition and are thought to exist functionally antagonistic, creating at differentiation and development-promoting loci what is termed a "bivalent domain" and rendering these genes sensitive to rapid induction or repression.[32]
Dna methylation [edit]
Regulation of gene expression is farther achieved through Dna methylation, in which the Deoxyribonucleic acid methyltransferase-mediated methylation of cytosine residues in CpG dinucleotides maintains heritable repression by controlling DNA accessibility.[32] The majority of CpG sites in embryonic stalk cells are unmethylated and appear to be associated with H3K4me3-carrying nucleosomes.[28] Upon differentiation, a small number of genes, including OCT4 and NANOG,[32] are methylated and their promoters repressed to prevent their further expression. Consistently, DNA methylation-deficient embryonic stalk cells apace enter apoptosis upon in vitro differentiation.[28]
Nucleosome positioning [edit]
While the Dna sequence of most cells of an organism is the same, the binding patterns of transcription factors and the corresponding factor expression patterns are different. To a large extent, differences in transcription factor bounden are determined by the chromatin accessibility of their bounden sites through histone modification and/or pioneer factors. In particular, it is important to know whether a nucleosome is roofing a given genomic bounden site or non. This can be determined using a chromatin immunoprecipitation (ChIP) assay.[33]
Histone acetylation and methylation [edit]
Deoxyribonucleic acid-nucleosome interactions are characterized by ii states: either tightly spring by nucleosomes and transcriptionally inactive, called heterochromatin, or loosely bound and unremarkably, but non always, transcriptionally active, called euchromatin. The epigenetic processes of histone methylation and acetylation, and their inverses demethylation and deacetylation primarily business relationship for these changes. The effects of acetylation and deacetylation are more predictable. An acetyl group is either added to or removed from the positively charged Lysine residues in histones by enzymes called histone acetyltransferases or histone deacteylases, respectively. The acetyl grouping prevents Lysine's clan with the negatively charged DNA backbone. Methylation is not equally straightforward, as neither methylation nor demethylation consistently correlate with either gene activation or repression. Nevertheless, certain methylations have been repeatedly shown to either actuate or repress genes. The trimethylation of lysine 4 on histone 3 (H3K4Me3) is associated with gene activation, whereas trimethylation of lysine 27 on histone three represses genes[34] [35] [36]
In stem cells [edit]
During differentiation, stem cells change their gene expression profiles. Recent studies have implicated a role for nucleosome positioning and histone modifications during this process.[37] There are two components of this process: turning off the expression of embryonic stem cell (ESC) genes, and the activation of cell fate genes. Lysine specific demethylase i (KDM1A) is thought to prevent the use of enhancer regions of pluripotency genes, thereby inhibiting their transcription.[38] It interacts with Mi-2/NuRD complex (nucleosome remodelling and histone deacetylase) complex,[38] giving an case where methylation and acetylation are non discrete and mutually exclusive, merely intertwined processes.
Role of signaling in epigenetic control [edit]
A concluding question to enquire concerns the part of cell signaling in influencing the epigenetic processes governing differentiation. Such a office should exist, equally it would be reasonable to think that extrinsic signaling tin lead to epigenetic remodeling, merely as it can pb to changes in gene expression through the activation or repression of unlike transcription factors. Lilliputian direct data is bachelor apropos the specific signals that influence the epigenome, and the bulk of current knowledge almost the subject consists of speculations on plausible candidate regulators of epigenetic remodeling.[39] We will showtime talk over several major candidates thought to be involved in the consecration and maintenance of both embryonic stalk cells and their differentiated progeny, and then plough to one example of specific signaling pathways in which more direct prove exists for its office in epigenetic change.
The start major candidate is Wnt signaling pathway. The Wnt pathway is involved in all stages of differentiation, and the ligand Wnt3a tin substitute for the overexpression of c-Myc in the generation of induced pluripotent stem cells.[39] On the other manus, disruption of β-catenin, a component of the Wnt signaling pathway, leads to decreased proliferation of neural progenitors.
Growth factors incorporate the second major fix of candidates of epigenetic regulators of cellular differentiation. These morphogens are crucial for evolution, and include os morphogenetic proteins, transforming growth factors (TGFs), and fibroblast growth factors (FGFs). TGFs and FGFs have been shown to sustain expression of OCT4, SOX2, and NANOG by downstream signaling to Smad proteins.[39] Depletion of growth factors promotes the differentiation of ESCs, while genes with bivalent chromatin can become either more restrictive or permissive in their transcription.[39]
Several other signaling pathways are too considered to exist primary candidates. Cytokine leukemia inhibitory factors are associated with the maintenance of mouse ESCs in an undifferentiated state. This is achieved through its activation of the Jak-STAT3 pathway, which has been shown to be necessary and sufficient towards maintaining mouse ESC pluripotency.[40] Retinoic acid can induce differentiation of man and mouse ESCs,[39] and Notch signaling is involved in the proliferation and self-renewal of stalk cells. Finally, Sonic hedgehog, in addition to its office every bit a morphogen, promotes embryonic stem cell differentiation and the self-renewal of somatic stem cells.[39]
The problem, of course, is that the candidacy of these signaling pathways was inferred primarily on the footing of their office in development and cellular differentiation. While epigenetic regulation is necessary for driving cellular differentiation, they are certainly not sufficient for this process. Direct modulation of gene expression through modification of transcription factors plays a key role that must be distinguished from heritable epigenetic changes that tin persist even in the absence of the original environmental signals. Merely a few examples of signaling pathways leading to epigenetic changes that alter cell fate currently be, and we will focus on i of them.
Expression of Shh (Sonic hedgehog) upregulates the product of BMI1, a component of the PcG complex that recognizes H3K27me3. This occurs in a Gli-dependent manner, as Gli1 and Gli2 are downstream effectors of the Hedgehog signaling pathway. In culture, Bmi1 mediates the Hedgehog pathway's ability to promote human mammary stem cell cocky-renewal.[41] In both humans and mice, researchers showed Bmi1 to exist highly expressed in proliferating immature cerebellar granule cell precursors. When Bmi1 was knocked out in mice, impaired cerebellar evolution resulted, leading to pregnant reductions in postnatal brain mass along with abnormalities in motor control and behavior.[42] A separate study showed a meaning decrease in neural stem prison cell proliferation along with increased astrocyte proliferation in Bmi cipher mice.[43]
An culling model of cellular differentiation during embryogenesis is that positional information is based on mechanical signalling past the cytoskeleton using Embryonic differentiation waves. The mechanical signal is then epigenetically transduced via signal transduction systems (of which specific molecules such equally Wnt are office) to effect in differential gene expression.
In summary, the role of signaling in the epigenetic control of cell fate in mammals is largely unknown, but distinct examples exist that indicate the likely being of further such mechanisms.
Effect of matrix elasticity [edit]
In order to fulfill the purpose of regenerating a diversity of tissues, developed stems are known to migrate from their niches, adhere to new extracellular matrices (ECM) and differentiate. The ductility of these microenvironments are unique to different tissue types. The ECM surrounding encephalon, musculus and os tissues range from soft to stiff. The transduction of the stem cells into these cells types is not directed solely by chemokine cues and cell to cell signaling. The elasticity of the microenvironment can also affect the differentiation of mesenchymal stem cells (MSCs which originate in bone marrow.) When MSCs are placed on substrates of the same stiffness as brain, muscle and bone ECM, the MSCs take on properties of those corresponding cell types.[44] Matrix sensing requires the cell to pull confronting the matrix at focal adhesions, which triggers a cellular mechano-transducer to generate a indicate to be informed what force is needed to deform the matrix. To make up one's mind the key players in matrix-elasticity-driven lineage specification in MSCs, different matrix microenvironments were mimicked. From these experiments, it was ended that focal adhesions of the MSCs were the cellular mechano-transducer sensing the differences of the matrix elasticity. The non-muscle myosin IIa-c isoforms generates the forces in the cell that atomic number 82 to signaling of early commitment markers. Nonmuscle myosin IIa generates the least forcefulness increasing to non-muscle myosin IIc. There are also factors in the cell that inhibit non-muscle myosin II, such as blebbistatin. This makes the cell effectively blind to the surrounding matrix.[44] Researchers have obtained some success in inducing stem cell-like properties in HEK 239 cells by providing a soft matrix without the use of diffusing factors.[45] The stalk-prison cell properties announced to be linked to tension in the cells' actin network. One identified machinery for matrix-induced differentiation is tension-induced proteins, which remodel chromatin in response to mechanical stretch.[46] The RhoA pathway is also implicated in this process.
Evolutionary history [edit]
A billion-years-erstwhile, probable holozoan, protist, Bicellum brasieri with two types of cells, shows that the evolution of differentiated multicellularity, possibly but not necessarily of animal lineages, occurred at to the lowest degree 1 billion years ago and perhaps mainly in freshwater lakes rather than the bounding main.[47] [48] [49] [ clarification needed ]
Run into also [edit]
- Interbilayer Forces in Membrane Fusion
- Fusion mechanism
- Lipid bilayer fusion
- Cell-jail cell fusogens
- CAF-ane
- List of homo prison cell types derived from the germ layers
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