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PubMed1992

[Spatial structure and antigenic activity of non-glycosylated forms of embryonal prealbumin-1 (EPA-1NG)].

The influence of temperature and pH on the spatial structure of EPA-1NG has been studied by means of circular dichroism and differential UV-spectroscopy, indicating the molecule to consist mainly of beta-structures. A conformational transition in the molecule was observed within the range of 40-50 degrees C. The further temperature elevation (up to 70 degrees C) was accompanied to the complete distortion of the parent conformation, which is reversed after cooling down to 20 degrees C. A correlation of the spectral data with the antigenic activity of genuine EPA-1NG and its carboxymethylated, heat-degraded and pH-denatured derivatives demonstrates that some antigenic determinants of EPA-1NG appear to be topographic.

Antigens↗

PubMed2003

Structure and disorder in the ribonuclease S-peptide probed by NMR residual dipolar couplings.

NMR residual dipolar couplings for the S-peptide of ribonuclease A aligned in C8E5/n-octanol liquid crystals are consistent with the presence of a native-like alpha-helix structure undergoing dynamic fraying. Residues 3-13, which correspond to the first alpha-helix of ribonuclease A, show couplings that become more negative at low temperature and in the presence of salt, conditions which stabilize alpha-helical structure in the S-peptide. By contrast, dipolar couplings from the N and C termini of the peptide are close to zero and remain nearly invariant with changes in solution conditions. Torsion angle dynamics simulations using a gradient of dihedral restraint bounds that increase from the center to the ends of the peptide reproduce the experimentally observed sequence dependence of dipolar couplings. The magnitudes of residual dipolar couplings depend on the anisotropy of the solute. Native proteins often achieve nearly spherical shapes due to the hydrophobic effect. Embryonic partially folded structures such as the S-peptide alpha-helix have an intrinsically greater potential for anisotropy that can result in sizable residual dipolar couplings in the absence of long-range structure.

1-Octanol↗

PubMed2006

Egr1 gene knockdown affects embryonic ocular development in zebrafish.

PURPOSE: To identify the changes in zebrafish embryonic ocular development after early growth response factor 1 (Egr1) gene knockdown by Egr1-specific translation inhibitor, morpholino oligonucleotides (MO). METHODS: Two kinds of Egr1-MO were microinjected separately with various dosages into one to four celled zebrafish embryos to find an optimal dose generating an acceptable mortality rate and high frequency of specific phenotype. Chordin-MO served as the positive control; a 5 mismatch MO of Egr1-MO1 and a nonspecific MO served as negative controls. We graded the Egr1 morphants according to their gross abnormalities, and measured their ocular dimensions accordingly. Western blot analysis and synthetic Egr1 mRNA rescue experiments confirmed whether the deformities were caused by Egr1 gene knockdown. Histological examination and three kinds of immunohistochemical staining were applied to identify glutamate receptor one expression in retinal ganglion cells and amacrine cells, to recognize acetylated alpha-tubulin expression which indicated axonogenesis, and to label photoreceptor cells with zpr-1 antibody. RESULTS: After microinjection of 8 ng Egr1-MO1 or 2 ng Egr1-MO2, 81.8% and 97.3% of larvae at 72 h postfertilization had specific defects, respectively. The gross phenotype included string-like heart, flat head, and deformed tail. The more severely deformed larvae had smaller eyes and pupils. Co-injection of 8 ng Egr1-MO1 and supplementary 12 pg synthetic Egr1 mRNA reduced the gross abnormality rate from 84.4% to 29.7%, and decreased the severity of deformities. Egr1 protein appeared in the wildtype and rescued morphants, but was lacking in the Egr1 morphants with specific deformities. Lenses of Egr1 morphants were smaller and had some residual nucleated lens fiber cells. Morphants' retinal cells arranged disorderly and compactly with thin plexiform layers. Immunohistochemical studies showed that morphants had a markedly decreased number of mature retinal ganglion cells, amacrine cells, and photoreceptor cells. Retinal axonogenesis was prominently reduced in morphants. CONCLUSIONS: The Egr1 gene plays an important role in zebrafish embryonic oculogenesis. Ocular structures including lens and retina were primitive and lacked appropriate differentiation. Such arrested retinal and lenticular development in Egr1 morphants resulted in microphthalmos.

Animals↗

PubMed1987

Subcortical rotation in Xenopus eggs: an early step in embryonic axis specification.

The amphibian egg undergoes a rotation of its subcortical cytoplasm relative to its surface during the first cell cycle. Nile blue spots applied to the egg periphery move with the subcortical cytoplasm and make rotation directly observable (J.-P. Vincent, G.F. Oster, and J. C. Gerhart (1986). Dev. Biol. 113, 484). We have previously shown that the direction of rotation accurately predicts the orientation of the embryonic axis developed by the egg. This suggests an important role for subcortical rotation in axis specification. In this report, we provide two kinds of experimental evidence for the essential role of rotation, and against a role for other concurrent cytoplasmic movements such as the convergence of subcortical cytoplasm toward the sperm entry point in the animal hemisphere. First, dispermic eggs develop only one embryonic axis, which is oriented accurately in line with the direction of the single rotation movement and not with the two convergence foci that form in the animal hemisphere. Rotation probably modifies the vegetal, not animal, hemisphere since axial development is normal in dispermic eggs despite highly altered animal subcortical movement. Second, we show that the amount of rotation correlates with the extent of dorsal development. UV irradiation of the vegetal hemisphere, or cold shock of the egg, inhibits rotation effectively. When there is no rotation, there is no dorsal development. On average within the egg population, increasing amounts of rotation correlate with the increasingly anterior limit of the dorsal structures of the embryonic body axis. However, individual partially inhibited eggs vary greatly in the amount of axis formed following a given amount of movement. Furthermore, the egg normally rotates more than is necessary for the development of a complete axis. These findings suggest that rotation, although essential, does not directly pattern the antero-posterior dimension of the body axis, but triggers a response system which varies from egg to egg in its sensitivity to rotation. This system is artificially sensitized by exposure of the egg to D2O shortly before rotation. We show that D2O-treated eggs produce extensive axes despite very limited rotation, often developing into hyperdorsal embryos. However, like normal eggs, they depend on rotation and cannot form dorsal structures if it is eliminated.

Animals↗

PubMedDate not supplied

Absence of bundle structure in the neocortex of the reeler mouse at the embryonic stage. Studies by scanning electron microscopic fractography.

The reeler mutant mouse is characterized by a derangement of the cerebral cortical structure due to abnormalities during the migration step at the embryonic stage. We have analyzed both the control and reeler cerebral cortex by means of scanning electron microscopic fractography. In the control cerebral cortex, the bundle formation was composed of fine fibers on which the migrating neuroblasts were attached perpendicular to the pial surface, whereas no bundle formation was observed in the reeler; instead, there was a fine meshwork of fibers surrounding the neuroblasts. The possible role of bundle formation in the normal cerebral cortex and the correlation between the inability of cells to migrate and the absence of bundle formation in the reeler is discussed.

Animals↗

PubMed2004

To die or not to die: the function of the transcription factor NF-kappaB in embryos exposed to stress.

BACKGROUND: Cytokines operating in the embryo and embryonic microenvironment determine, to a significant extent, whether pregnancy is completed successfully or results in embryonic loss or maldevelopment. They act as activators of specific transcription factors, which control cell responses such as cell proliferation differentiation and apoptosis. One such transcription factor is the nuclear factor-kappaB (NF-kappaB), which is presently seen as a key molecule controlling the apoptosis process. In the light of evidence that a majority of embryopathic stresses, regardless of their nature, first disturb the apoptotic process, it is conceivable, that NF-kappaB may play an important role in regulating the resistance of embryos to embryopathic stresses. In this brief review, we discuss such a possibility based on data characterizing expression and function of NF-kappaB in the embryo and extraembryonic tissues during normal embryogenesis as well as after exposure to various embryopathic stresses. METHODS: Critical review of existing data. RESULTS: Data summarized in this review suggest that (a) practically all NF-kappaB/Rel family members are expressed in embryonic, trophoblast and uterine cells in a developmental stage- and cell type-specific manner; (b) NF-kappaB-mediated anti-apoptotic signaling in embryonic cells seems to be indispensable for proper development during the organogenesis stage, (c) NF-kappaB activity in stress-targeted embryonic and extraembryonic structures directly correlates with their ability to resist stress-induced process of embryo loss and maldevelopment. CONCLUSION: Data presented in this review suggest that NF-kappaB may act as a protector of embryos exposed to embryopathic stresses, possibly, because of the ability of NF-kappaB to prevent the induction of programmed cell death as well as to activate cell proliferation.

Apoptosis↗

PubMed1997

Both apolipoprotein E and A-I genes are present in a nonmammalian vertebrate and are highly expressed during embryonic development.

Apolipoprotein E (apoE) is associated with several classes of plasma lipoproteins and mediates uptake of lipoproteins through its ability to interact with specific cell surface receptors. Besides its role in cardiovascular diseases, accumulating evidence has suggested that apoE could play a role in neurodegenerative diseases, such as Alzheimer disease. In vertebrates, apoA-I is the major protein of high-density lipoprotein. ApoA-I may play an important role in regulating the cholesterol content of peripheral tissues through the reverse cholesterol transport pathway. We have isolated cDNA clones that code for apoE and apoA-I from a zebrafish embryo library. Analysis of the deduced amino acid sequences showed the presence of a region enriched in basic amino acids in zebrafish apoE similar to the lipoprotein receptor-binding region of human apoE. We demonstrated by whole-mount in situ hybridization that apoE and apoA-I genes are highly expressed in the yolk syncytial layer, an extraembryonic structure implicated in embryonic and larval nutrition. ApoE transcripts were also observed in the deep cell layer during blastula stage, in numerous ectodermal derivatives after gastrulation, and after 3 days of development in a limited number of cells both in brain and in the eyes. Our data indicate that apoE can be found in a nonmammalian vertebrate and that the duplication events, from which apoE and apoA-I genes arose, occurred before the divergence of the tetrapod and teleost ancestors. Zebrafish can be used as a simple and useful model for studying the role of apolipoproteins in embryonic and larval nutrition and of apoE in brain morphogenesis and regeneration.

Amino Acid Sequence↗

PubMed1997

The XHex homeobox gene is expressed during development of the vascular endothelium: overexpression leads to an increase in vascular endothelial cell number.

The Hex/Prh homeobox gene is expressed in a subset of adult blood cell types and may play a role in the differentiation of the myeloid and B-cell lineages. In a search for homeobox genes involved in cardiovascular development, we have independently isolated a Xenopus laevis cDNA which appears to be the amphibian orthologue of Hex/Prh. Based on high sequence similarity in a number of regions, particularly the critical homeobox, we have named this gene XHex. This developmentally regulated gene is first expressed in the dorsal endomesoderm of the gastrula stage embryo. This tissue goes on to contribute to the structures of the embryonic liver and XHex continues to be expressed in the liver throughout development. From the tailbud stage, XHex is expressed in vascular endothelial cells throughout the developing vascular network. Vascular expression of XHex is transient and commences slightly after expression of the receptor tyrosine kinase gene, flk-1, which is known to be essential for vascular development. This observation raises the possibility that XHex is one of the transcription factors that responds to the VEGF/Flk-1 signal transduction pathway leading to differentiation of vascular endothelial cells. XHex is unique amongst homeobox genes in displaying expression in the endothelial layer throughout the developing vasculature. Overexpression of XHex sequences in the frog embryo causes disruption to developing vascular structures and an increase in the number of vascular endothelial cells, suggesting a possible role in regulation of cell proliferation.

Amino Acid Sequence↗

PubMed1996

Inactivation of the mouse Brca1 gene leads to failure in the morphogenesis of the egg cylinder in early postimplantation development.

BRCA1 is proposed to be a tumor suppressor gene. To explore the biological function of BRCA1, a partial deletion (amino acids 300-361) of mouse Brca1 exon 11 was introduced into the genome of embryonic stem (ES) cells by homologous recombination. Mice carrying one mutated allele of Brca1 appear normal and are fertile up to 10 months of age without any sign of illness. However, no viable progeny homozygous for the Brca1 mutant allele were obtained. Detailed analysis of large numbers of embryos at different stages of development indicated that the homozygous mutant concepti are severely retarded in growth as early as embryonic day 4.5 (E4.5) and are resorbed completely by E8.5. Although the homozygotes at E5.5-E6.5 are able to synthesize DNA and display distinguishable embryonic and extraembryonic structures, they fail to differentiate and form egg cylinders. Consequently, they were unable to form primitive streaks and undergo gastrulation. Consistent with these in vivo results, blastocysts homozygous for mutated Brca1 alleles are at a considerable disadvantage when grown in vitro. These observations suggest that Brca1 has an important role in the early development of mouse embryos.

Animals↗

PubMed2000

Temporospatial patterns of apoptosis in chick embryos during the morphogenetic period of development.

We examined the temporospatial pattern of naturally occurring apoptosis in chick embryos to five days of incubation (H.H. stages 1-25; Hamburger and Hamilton, 1951) using TUNEL labeling. The initial TUNEL-positive structure was the embryonic shield at stage 1. Apoptotic cells became ubiquitously present within embryos by stage 3, which is early in gastrulation. Until stage 6, TUNEL-positive cells were restricted to the headfold region. In embryos of stages 7-8, most cell death was localized at the most anterior neural plate. TUNEL-positive neural plate, notochord and somites appeared at stage 9. Otic and optic regions became TUNEL-positive at stage 11. The aggregation of cells from which the tail bud arises contains apoptotic cells from stage 11 onwards. At stage 16, scattered TUNEL-positive cells appeared in the branchial arches. Three streams of apoptotic neural crest cells in the cranial region became most clearly visible at stage 18. The secondary neural tube from which caudal structures develop contains apoptotic cells at stage 14. Apoptotic cells are present in the branchial arches and lateral body wall for extended periods, stages 16-25 and 25 respectively. At stages 24-25, intense positive regions of cell death were confined to the caudal regions of the arches, to limb and tail buds and to the lateral body wall, the latter in relation to body wall closure. The new findings in this study are discussed along with past studies to provide the temporospatial pattern of cell death during early chick development.

Animals↗

PubMed1975

Median facial malformations and their implications for brain malformations.

For purposes of identifying craniofacial syndromes which predict brain malformations the face can be regarded as developing from 2 sources. The median and paramedian structures derive from the embryonic segment of the face, termed the frontonasal prominence. The lateral structures of the face derive from the branchial arches. Certain patterns of median plane facial anomalies predict a severe brain malformation, while other patterns, although producing equally grotesque facial malformations, bear little association with a malformed brain. Orbital hypotelorism may occur in a variety of syndromes with microcephaly. When combined in typical patterns with other median plane facial defects, the patient almost certainly has holoprosencephaly, and has a poor prognosis for useful psychomotor development and survival. To the current knowledge of the author, every patient with orbital hypotelorism and total aplasia of the intermaxillary segment has a severely malformed brain. These patients, with only a rare exception, make no useful psychomotor progress and die in infancy. Orbital hypertelorism implies an increased risk of a neurologically abnormal patient, but neither the mental deficiency nor the prognosis for survival are as poor as in hypotelorism. When hypertelorism is combined with certain median plane facial anomalies the patient has the median cleft face syndrome and most likely has normal mentality, or only mild retardation, and has a normal prognosis for survival.

Abnormalities, Multiple↗

PubMed2005

Possible role of Rho/Rhotekin signaling in mammalian septin organization.

There is growing evidence for crosstalk between septin filaments and actin cytoskeleton which is regulated by Rho family of GTPases. Here we show that active Rho disrupts septin filament structures in rat embryonic fibroblast REF52 cells. Among Rho effector molecules tested, Rhotekin induced morphological changes of septin filaments similar to those by activated Rho. The center region of Rhotekin was sufficient for the septin reorganization in the cells, and likely to interact indirectly with the C-terminal half of a septin Sept9b, where a GTPase domain is located. Rhotekin and Sept9b are colocalized mainly in perinuclear regions in serum-starved REF52 cells. Upon stimulation with lysophosphatidic acid, they translocated to actin stress fibers in 10 min and then redistributed again to cytoplasm after 90 min treatment. In neuroblastoma Neuro2a cells, Rhotekin and Sept9b were enriched in the tip of neurites, a location where cortical actin reorganization is induced upon stimulation with lysophosphatidic acid. Taken together, we propose that Rhotekin is a novel regulator organizing mammalian septin structures and provide a new link between the septin and Rho-signaling.

Actins↗

PubMed2000

Effect of prenatal stress on proliferative activity and chromosome aberrations in embryo brain in rats with different excitability of the nervous system.

Stress during pregnancy affects the morphogenesis of embryonal brain, its structural and functional characteristics, and behavior of the progeny. Genetic mechanisms of this process remain unclear. Cytogenetic characteristics of neuroblasts were analyzed in 17-18-day embryos of rats selected by threshold excitability of the nervous system in health and after emotional painful stress during the third trimester of pregnancy. The strains differed by the effect of stress on proliferative activity and chromosome aberrations in cells of the future hippocampus depending on the strain-specific characteristics of the nervous system excitability. This effect is regarded as an important component of epigenetic regulation of neurogenesis and behavior.

Animals↗

PubMed2004

BASP1 is a transcriptional cosuppressor for the Wilms' tumor suppressor protein WT1.

The Wilms' tumor suppressor protein WT1 is a transcriptional regulator that plays a key role in the development of the kidneys. The transcriptional activation domain of WT1 is subject to regulation by a suppression region within the N terminus of WT1. Using a functional assay, we provide direct evidence that this requires a transcriptional cosuppressor, which we identify as brain acid soluble protein 1 (BASP1). WT1 and BASP1 associate within the nuclei of cells that naturally express both proteins. BASP1 can confer WT1 cosuppressor activity in transfection assays, and elimination of endogenous BASP1 expression augments transcriptional activation by WT1. BASP1 is present in the developing nephron structures of the embryonic kidney and, coincident with that of WT1, its expression is restricted to the highly specialized podocyte cells of the adult kidney. Taken together, our results show that BASP1 is a WT1-associated factor that can regulate WT1 transcriptional activity.

Adult↗

PubMed2004

The apical disposition of the Caenorhabditis elegans intestinal terminal web is maintained by LET-413.

We wish to understand how organ-specific structures assemble during embryonic development. In the present paper, we consider what determines the subapical position of the terminal web in the intestinal cells of the nematode Caenorhabditis elegans. The terminal web refers to the organelle-depleted, intermediate filament-rich layer of cytoplasm that underlies the apical microvilli of polarized epithelial cells. It is generally regarded as the anchor for actin rootlets protruding from the microvillar cores. We demonstrate that: (i) the widely used monoclonal antibody MH33 reacts (only) with the gut-specific intermediate filament protein encoded by the ifb-2 gene; (ii) IFB-2 protein accumulates near the gut lumen beginning at the lima bean stage of embryogenesis and remains associated with the gut lumen into adulthood; and (iii) as revealed by immunoelectron microscopy, IFB-2 protein is confined to a discrete circumferential subapical layer within the intestinal terminal web (known in nematodes as the "endotube"); this layer joins directly to the apical junction complexes that connect adjacent gut cells. To investigate what determines the disposition of the IFB-2-containing structure as the terminal web assembles during development, RNAi was used to remove the functions of gene products previously shown to be involved in the overall apicobasal polarity of the developing gut cell. Removal of dlg-1, ajm-1, or hmp-1 function has little effect on the overall position or continuity of the terminal web IFB-2-containing layer. In contrast, removal of the function of the let-413 gene leads to a basolateral expansion of the terminal web, to the point where it can now extend around the entire circumference of the gut cell. The same treatment also leads to concordant basolateral expansion of both gut cell cortical actin and the actin-associated protein ERM-1. LET-413 has previously been shown to be basolaterally located and to prevent the basolateral expansion of several individual apical proteins. In the present context, we conclude that LET-413 is also necessary to maintain the entire terminal web or brush border assembly at the apical surface of C. elegans gut cells, a dramatic example of the so-called "fence" function ascribed to epithelial cell junctions. On the other hand, LET-413 is not necessary to establish this apical location during early development. Finally, the distance at which the terminal web intermediate filament layer lies beneath the gut cell surface (both apical and basolateral) must be determined independently of apical junction position.

Animals↗

PubMed1976

Chick cytoplasmic actin and muscle actin have different structural genes.

Actins isolated from embryonic chick brain and muscle differ in mobility when subjected to electrophoresis in gels containing urea and sodium dodecyl sulfate. Experiments were carried out to determine whether these actins are products of different structural genes and differ in primary amino acid sequence, or whether they are products of the same structural gene but are different because of post-translational modification. Messenger RNA from brain and muscle tissue was used to direct cell-free protein synthesis in wheat germ extracts. The synthesized actins were identified by conversion from globular to fibrous actin and by two-dimensional chromatographic analysis of tryptic peptides. The differences in electrophoretic mobility of brain compared to muscle actin were maintained in the cell-free protein synthetic products. Therefore, these mobility differences were not due to post-translational modification. It was concluded that brain and muscle actin are coded by different messenger RNAs and therefore arise from different structural genes. In addition, messenger RNA from 13- and 16-day embryonic thigh muscle directed the synthesis of both brain- and muscle-type actins, suggesting that muscle cell differentiation involves the regulation of at least two different actin genes.

Actins↗

PubMed1980

[The information content of intracellular water and its accumulation in embryo- and phylogenesis (author's transl)].

The nucleo-free erythrocytes is presented as the simplest differentiated cell whose energy-exchange has the single purpose of preserving the cell structure; this structure is based on the regular quasi-crystalline state of intracellular water, which is expressed by the negative entropy (-SW) and the temperature TW which is higher than the temperature of the extracellular water T. The information content of intracellular water, JW is proportional to the temperature difference: JW approximately delta T = TW - T. The regular state of intracellular water is maintained by the basal metabolism that takes place in the membrane of the differentiated cell. The energy exchange, i.e., the absorption of free energy and the liberation of an equivalent amount of heat, occurs in the form of work cycles of the enzyme-water-complexes in the cell membrane. The differentiated cell of the multicellular animal organism is the result of embryogenetic processes accompanied by heat-liberation. The specific heat-liberation, i.e., the heat produced by a single cell, begins with a quasi-zero value of the fertilized egg cell and grows with acceleration to a maximum value at the end of embryogenesis. This process of acceleration of heat-liberation is caused by the entrance of the water from the outer medium into the embryonic cell; the water undergoes the phase-change "fluid yields crystal" with heat-liberation. The intracellular water within the embryonic cell becomes structurated; this is also accompanied by growing heat-liberation. The thermodynamic characteristic of embryo genetic development is expressed by the principle of the maximum of velocity of entropy production of the cell at the end state of the process of differentiation. This principle applied to phylogenetics, leads to the formulation of the principle of accumulation of biological information: J(t). In the course of evolution living systems are able not only to store information of past generations, but also to create information: J(t) approximately e-1nt1!, where t is the time of phylogenesis.

Animals↗

PubMed1995

Gradient of integrin alpha 6A distribution in the myocardium during early heart development.

The interactions of cells with extracellular matrices (ECM)1 are likely to be key determinants of embryonic development. Integrin adhesion receptors are ideally positioned to mediate some of these interactions since, in addition to mechanical adhesion, they transduce signals affecting cell proliferation and differentiation. We investigated expression of the integrin alpha 6 beta 1, a receptor for the ECM component, laminin in the early mouse embryo. An intriguing feature of this integrin is the existence of alpha 6 subunit isoforms. The A and B isoforms, which differ in the cytoplasmic tails, are expressed in cell-type specific fashion, and are likely to implement distinct cellular interactions with laminin. By RT-PCR, alpha 6B but not alpha 6A mRNA was detectable in embryo extracts from fertilized oocytes to 6.5 d.p.c. In subsequent stages, up to 11.5 d.p.c., alpha 6A mRNA was observed in mRNA extracts from whole embryos, but still in significantly lower amounts than alpha 6B. However, in extracts from isolated heart (9.5 to 11.5 d.p.c.), alpha 6A was the predominant alpha 6 isoform, while in extracts from other embryo parts no alpha 6A mRNA was detectable. At the protein level, immunostaining with specific antibodies showed alpha 6A protein in myocardial cells, at the early stage of heart tube development (8.5 d.p.c.). Localization to the myocardium was tightly restricted, since other structures of the embryonic heart, e.g., endocardium, or of the remaining embryo did not stain with anti-alpha 6A antibody. In the ventricular myocardium, expression of alpha 6A appeared more intense than in the subendocardial layer. Quantitation by confocal microscopy unveiled a gradient of expression of alpha 6A, increasing from the outer to the inner layers of the myocardium. This is the first demonstration of a gradient distribution of integrin molecules in a tissue, which appears to be directly connected with the process of organogenesis. The mechanism underlying our observations is not the turning on of a gene, rather it is the activation of a splicing mechanism that substitutes the cytoplasmic domain of a laminin receptor. Because integrin cytoplasmic domains are thought to be an important functional end of the molecule, this may be a mechanism to modulate cellular responses to laminin.

Animals↗