Biomedical subjects

Wood Yee Chan

Publications and source records attributed to Wood Yee Chan.

15 recordsLinked to original sources

PubMed2006

S100A1-deficient male mice exhibit increased exploratory activity and reduced anxiety-related responses.

S100 proteins comprise a family of Ca(2+) binding proteins of at least 21 members. They are distinctly expressed in a variety of cell types and tissues and are thought to play unique roles, although they share a high degree of sequence homology and expression overlap. S100A1 is prominently expressed in the heart, where it takes part in Ca(2+)-cycling. Its role in the central nervous system (CNS) is largely unknown. We have generated S100A1-deficient mice by gene trap mutagenesis to study the involvement of S100A1 in the cytoarchitecture of the brain, in learning and memory, and in avoidance-approach behavior. S100A1 knock out (KO) mice develop well and their brains present with normal morphology. In wild type (Wt) mice, S100A1 protein was found in the hippocampus, cerebral cortex and amygdala, and partially co-localized with the astrocyte marker glial fibrillary acidic protein (GFAP) in the stratum radiatum of the hippocampus. Astrocytes and neurons of S100A1KO mice did not differ from those of Wt mice regarding shape, distribution and density. In the water maze, S100A1KO mice performed equally well as Wt, implying that S100A1 is not involved in spatial learning and memory. In avoidance-approach tests, predominantly male S100A1KO mice showed reduced anxiety-like responses and enhanced explorative activities. We conclude that S100A1 plays a role in modulating innate fear and exploration of novel stimuli.

Animals↗

PubMed2006

Thrombopoietin protects against in vitro and in vivo cardiotoxicity induced by doxorubicin.

BACKGROUND: Doxorubicin (DOX) is an important antineoplastic agent. However, the associated cardiotoxicity, possibly mediated by the production of reactive oxygen species, has remained a significant and dose-limiting clinical problem. Our hypothesis is that the hematopoietic/megakaryocytopoietic growth factor thrombopoietin (TPO) protects against DOX-induced cardiotoxicity and might involve antiapoptotic mechanism exerted on cardiomyocytes. METHODS AND RESULTS: In vitro investigations on H9C2 cell line and spontaneously beating cells of primary, neonatal rat ventricle, as well as an in vivo study in a mouse model of DOX-induced acute cardiomyopathy, were performed. Our results showed that pretreatment with TPO significantly increased viability of DOX-injured H9C2 cells and beating rates of neonatal myocytes, with effects similar to those of dexrazoxane, a clinically approved cardiac protective agent. TPO ameliorated DOX-induced apoptosis of H9C2 cells as demonstrated by assays of annexin V, active caspase-3, and mitochondrial membrane potential. In the mouse model, administration of TPO (12.5 microg/kg IP for 3 alternate days) significantly reduced DOX-induced (20 mg/kg) cardiotoxicity, including low blood cell count, cardiomyocyte lesions (apoptosis, vacuolization, and myofibrillar loss), and animal mortality. Using Doppler echocardiography, we observed increased heart rate, fractional shortening, and cardiac output in animals pretreated with TPO compared with those receiving DOX alone. CONCLUSIONS: These data have provided the first evidence that TPO is a protective agent against DOX-induced cardiac injury. We propose to further explore an integrated program, incorporating TPO with other protocols, for treatment of DOX-induced cardiotoxicity and other forms of cardiomyopathy.

Animals↗

PubMed2006

Immunohistological evidences of Ginkgo biloba extract altering Bax to Bcl-2 expression ratio in the hippocampus and motor cortex of senescence accelerated mice.

Ginkgo biloba extract 761 appears to display neuroprotective effect in many nervous diseases and aging. Deterioration of mental functions during aging is always accompanied by loss of neurons, presumably through apoptosis. Here, we studied the effect of G. biloba extract in the expression of Bax/Bcl-2 ratio, an important apoptotic index, in the hippocampus and motor cortex of the aging brain. Bax and Bcl-2 expressions were examined with immunohistochemical methods. Senescence Accelerated Mice Prone Strain 8 was used because the aging process was accelerated with neuropathological alterations similar to those found in the aging human brain. The mice were fed with either G. biloba extract or sucrose from the age of 3 weeks until sacrifice at 3 or 9 months old. In the hippocampus of G. biloba fed 9-month-old mice, the ratio of Bax positive cell to Bcl-2 positive cell (Bax/Bcl-2 expression ratio) was 11.43 +/- 3.11 (mean +/- SD); significantly lower (P < 0.05) than the Bax/Bcl-2 expression ratio of 20.99 +/- 5.34 in the sucrose fed mice. The Bax/Bcl-2 expression cell ratios, however, in the motor cortex were not significantly different between the two groups (2.22 +/- 1.35 versus 2.27 +/- 2.02 for the G. biloba and the sucrose fed mice, respectively). The decrease in the Bax/Bcl-2 expression cell ratio following G. biloba treatment might hence be able to protect the aging hippocampus from moving further down the apoptotic pathway. Western blotting confirmed the decrease of Bax in the brain even after a short term and high dose Ginkgo treatment. It is speculated that the G. biloba extract may be a potential neuroprotective agent against apoptosis through the differential expressions of the Bax and Bcl-2 in the hippocampus.

Animals↗

PubMed2005

Partial neuroprotective effect of pretreatment with tanshinone IIA on neonatal hypoxia-ischemia brain damage.

Tanshinone IIA is a compound purified from the Chinese herb Danshen (Radix Salviae Miltiorrhiza Bge). The neuroprotective effect of tanshinone IIA was investigated in a neonatal rat model of hypoxia-ischemia brain damage. Hypoxia-ischemia encephalopathy was induced in rats at day 7 of postnatal age by ligation of the right common carotid artery, followed by 2 h of hypoxia. Tanshinone IIA (10 mg/kg, i.p.) was injected daily from day 2 before surgery for 9 or 16 d. Our results demonstrated significant and sustained brain damage in the hypoxia-ischemia- and vehicle-treated groups at 1 and 3 wk after surgery. Treatment with tanshinone IIA significantly reduced the severity of brain injury, as indicated by the increase in ipsilateral brain weight and neuron density, compared with those of sham-operated animals. The recovery of sensorimotor function and histology was observed in animals that received tanshinone IIA. The plasma of tanshinone IIA-treated rats exhibited higher antioxidant activities, as reflected by the oxygen radical absorbance capacity assay, compared with the vehicle-treated rats. In the neural progenitor cell line C17.2 that was subjected to 2,2'-azobis (2-amidino propane hydrochloride)-induced oxidative stress, tanshinone IIA increased cell viability and protected against mitochondrial damage (JC-1 assay). Our results suggest that tanshinone IIA has antioxidative activities and that treatment that is started before a hypoxic-ischemic insult is partially neuroprotective. Further studies are required to elucidate whether rescue treatment with tanshinone IIA is effective and to determine whether its protective effect is also associated with secondary cooling of the brain.

Abietanes↗

PubMed2004

Expression patterns of PSA-NCAM in the human ganglionic eminence and its vicinity: role of PSA-NCAM in neuronal migration and axonal growth?

The ganglionic eminence (GE) is a transient but conspicuous structure of the developing forebrain which not only gives rise to a large number of precursor neurons and glial cells for various structures of the forebrain, but in addition serves as an intermediate target for growing axons to the cerebral cortex. To investigate the roles of the highly polysialylated isoform of the neural cell adhesion molecule (PSA-NCAM) in cell migration and axonal growth within the GE and its neighbouring structures, the spatio-temporal expression pattern of PSA-NCAM was examined in human fetal forebrains between 14 and 36 weeks of gestation with a specific immunohistochemical method. Scattered PSA-NCAM-positive cells were found in the centre but more frequently in the marginal zone of the GE. Intensely labelled cells were also identified in the gangliothalamic body, basolateral nuclei of the amygdala and the subventricular and intermediate zone adjacent to the GE. This cellular immunoreactivity started to appear in various structures during the period from 14 to 19 weeks and gradually diminished after 25-28 weeks. Strong immunoreactivity was also detected in fibres running from the intermediate zone of the neocortex to the internal capsule from 16 weeks onwards, and after 24 weeks, the immunoreactivity was gradually decreased. In the vicinity of the GE, between 16 and 22 weeks, short fibre bundles were observed to leave the longitudinally oriented axons of the internal capsule to reach the marginal zone of the GE. Our results suggest a close relationship between PSA-NCAM expression and neuronal migration (over short distances) and transitory axonal projections (target recognition and axonal fasciculation) in the region of the GE.

Axons↗

PubMed2004

Cardiac neural crest of the mouse embryo: axial level of origin, migratory pathway and cell autonomy of the splotch (Sp2H) mutant effect.

A sub-population of the neural crest is known to play a crucial role in development of the cardiac outflow tract. Studies in avians have mapped the complete migratory pathways taken by 'cardiac' neural crest cells en route from the neural tube to the developing heart. A cardiac neural crest lineage is also known to exist in mammals, although detailed information on its axial level of origin and migratory pattern are lacking. We used focal cell labelling and orthotopic grafting, followed by whole embryo culture, to determine the spatio-temporal migratory pattern of cardiac neural crest in mouse embryos. Axial levels between the post-otic hindbrain and somite 4 contributed neural crest cells to the heart, with the neural tube opposite somite 2 being the most prolific source. Emigration of cardiac neural crest from the neural tube began at the 7-somite stage, with cells migrating in pathways dorsolateral to the somite, medial to the somite, and between somites. Subsequently, cardiac neural crest cells migrated through the peri-aortic mesenchyme, lateral to the pharynx, through pharyngeal arches 3, 4 and 6, and into the aortic sac. Colonisation of the outflow tract mesenchyme was detected at the 32-somite stage. Embryos homozygous for the Sp2H mutation show delayed onset of cardiac neural crest emigration, although the pathways of subsequent migration resembled wild type. The number of neural crest cells along the cardiac migratory pathway was significantly reduced in Sp2H/Sp2H embryos. To resolve current controversy over the cell autonomy of the splotch cardiac neural crest defect, we performed reciprocal grafts of premigratory neural crest between wild type and splotch embryos. Sp2H/Sp2H cells migrated normally in the +/+ environment, and +/+ cells migrated normally in the Sp2H/Sp2H environment. In contrast, retarded migration along the cardiac route occurred when either Sp2H/+ or Sp2H/Sp2H neural crest cells were grafted into the Sp2H/Sp2H environment. We conclude that the retardation of cardiac neural crest migration in splotch mutant embryos requires the genetic defect in both neural crest cells and their migratory environment.

Animals↗

PubMed2003

Development of catecholaminergic neurons in the human medulla oblongata.

Distribution and maturation of catecholaminergic (CA) neurons have been studied by tyrosine hydroxylase immunohistochemistry in the medulla oblongata of human fetuses aged 14.5-25 weeks of gestation. Already at 14.5 weeks, CA neurons were observed in two longitudinally oriented cell clusters, one located ventrolaterally in the area of the lateral reticular and ambiguous nuclei, the other one dorsomedially forming 4 groups related to the dorsal vagal nucleus, the commissural nucleus of the vagus, the nucleus of the tractus solitarius and the area postrema. CA neurons in the area postrema were often found close to blood vessels. Scattered intermediate CA neurons were seen between these two larger clusters. CA neurons still appeared immature exhibiting bipolar morphology with only one or two short stout processes, which hardly branched. At 21 weeks, CA neurons occupied essentially the same location, but had a more mature morphology. Though still bipolar in shape, they had thinner and much longer processes which frequently branched. Both in the ventrolateral and the dorsomedial cell clusters, these processes were frequently lying close to blood vessels. At 25 weeks, CA cells had matured into multipolar neurons with long thin processes forming fine fiber networks in the ventrolateral medulla as well as around and within the dorsal vagal and solitarius nuclei. Only at this stage, a distinct CA fiber tract was seen located in the region of the tractus solitarius. Our results indicate that CA neurons in the human medulla, which are presumably involved in the control of ventilation and blood pressure, though generated rather early during development, mature relatively late.

Adult↗

PubMed2003

Receptor-mediated endocytosis of trichosanthin in choriocarcinoma cells.

Trichosanthin (TCS) is a ribosome inactivating protein (RIP). It is generally believed that its many biological activities act through inhibition of ribosomes resulting in a decrease in protein synthesis. It has been hypothesized that the rate of entry of TCS into cells to reach ribosomes is an important factor in determining its biological activity. To prove this hypothesis, we have mapped out and compared the intracellular routing of TCS in two cell lines, namely the choriocarcinoma JAR cell line, which is known to be highly sensitive to the toxic effects of TCS, and the hepatoma H35 cell line, to which TCS shows minimal toxicity. Results from laser scanning confocal microscopy indicated that fluorescein isothiocyanate labeled TCS quickly accumulated inside JAR cells within 4 h of incubation while only a low level of fluorescent signals was detected in H35 cells during the same period of time. When TCS was conjugated with gold particles (Au) and its intracellular locations were traced with a transmission electron microscope, it was found that most of TCS were bound to coated pits on the JAR cell surface and were rapidly internalized within an hour. By 4 h, TCS reached almost every cytoplasmic region including ribosomes, and the JAR cell began to degenerate. In H35 cells, however, the binding of TCS to coated pits was not observed, but instead, a small amount of TCS was found to penetrate the cell non-specifically by direct diffusion across the cell membrane. Our observations suggest that most of TCS enter JAR cells via a specific receptor mediated pathway, which allows a swift transport of TCS across the membrane and a rapid accumulation of intracellular TCS, while in H35 cells, TCS takes a slow and non-specific route. The receptor-mediated uptake together with the specific intracellular routing of TCS may partly account for the differential vulnerability of the choriocarcinoma cell line towards the toxicity of TCS.

Animals↗

PubMed2003

Differential expression of S100 proteins in the developing human hippocampus and temporal cortex.

S100 calcium binding proteins have long been known to express in the adult nervous system, but their distribution in the developing brain, especially the human fetal brain, is largely unknown. We used an immunohistochemical method to determine the expression of three S100 proteins, namely S100A4, S100A5, and S100A13, in the human fetal hippocampus and temporal cortex from 12 to 33 weeks of gestation. At 12 weeks, S100A5 was strongly expressed in the cells and fibers of the polymorphic, pyramidal, and molecular layers of the hippocampus. Thereafter, its expression decreased with age. In the temporal cortex, S100A5 expression was detected from 12 weeks onwards, peaked at 20 to 24 weeks, and then decreased with age. The horizontal fibers of the marginal zone were immunoreactive at all stages examined. S100A13 immunoreactivity was also detected in both cells and fibers of the hippocampus at 12 weeks, became slightly stronger at 20 weeks, and then decreased with age. In the temporal cortex, S100A13 immunoreactivity was also strong in all cellular layers at 12 to 24 weeks before it declined with age from 28 weeks onwards. Among the three proteins examined, S100A4 showed the weakest expression, which was detected in the cells and fibers of the hippocampus and the temporal cortex at all stages examined. Our results have demonstrated for the first time, in the human fetal hippocampus and temporal cortex, specific spatio-temporal patterns of expression of these proteins, all of which are likely to have different roles to play during development despite their pronounced sequence homology.

Fetus↗

PubMed2003

Development of the human cerebral cortex: a histochemical study.

In recent years, improvement in diagnostic techniques has led to better recognition of "disorders of cortical development". These disorders constitute a significant cause of epilepsy, mental retardation, developmental delay and neurological deficits in childhood, and may also contribute to the pathogenesis of psychological and neurodegenerative diseases in adults. Hitherto, however, few systematic studies of the human fetal cortex have been performed, and little is known about the ontogenetic processes of the neocortex in man. The aim of the study is to establish an understanding of the developmental events that occur in the second and third trimesters of gestation, by investigating the biochemical patterns of development of the human neocortex during this period. The temporal and spatial patterns of expression of the neuronal markers gamma-aminobutyric acid (GABA), choline acetyltransferase (ChAT), dopamine beta hydroxylase (DBH), dopamine receptor DR1 and synaptophysin, as well as the glial cell markers glial fibrillary acidic protein (GFAP), S100B and excitatory amino acid transporter protein GLT-1 are delineated in the fetal cortex using immunohistochemistry. Results of this study showed that different neuronal and glial cell proteins follow different developmental patterns and many show inter- or intra-regional variations in expression. Details of these patterns are described and discussed. The early expression of these proteins suggests that they play important roles in the developmental processes of cell proliferation, migration and differentiation. Both neurotransmitters and glial cell proteins probably function outside the confines of synapses in the fetal brain, as paracrine/autocrine factors. Early developmental events seem to be dictated by an innate programme, whereas late events may be more susceptible to extrinsic influences. It is hoped that knowledge of the normal developmental process can lead to better understanding of the causes and mechanisms of "disorders of cortical development", and to better treatments.

Acetylcholine↗

PubMed2003

Early postnatal sound exposure induces lasting neuronal changes in the inferior colliculus of senescence accelerated mice (SAMP8): a morphometric study on GABAergic neurons and NMDA expression.

Senescence-acceleration-prone mice (SAMP8) provide a model to study the influence of early postnatal sound exposure upon the aging auditory midbrain. SAMP8 were exposed to a 9-kHz monotone of either 53- or 65-dB sound pressure level during the first 30 postnatal days, the neurons in the auditory midbrain responding selectively to 9 kHz were localized by c-fos immunohistochemistry and the following parameters were compared to control SAMP8 not exposed to sound: mortality after sound exposure, dendritic spine density, and quantitative neurochemical alterations in this 9-kHz isofrequency lamina. For morphometric analysis, animals were examined at 1, 4, and 8 months of age. Serial sections of the inferior colliculus were Golgi impregnated or stained immunohistochemically for the expression of epsilon1 subunit of NMDA receptor or GABA. Mortality after exposure to 53 dB was the same as in controls, but was markedly increased from 7 months of age onward after postnatal exposure to 65 dB. No gross morphological alterations were observed in the auditory midbrain after sound exposure. However, sound exposure to 53 or 65 dB significantly reduced dendritic spine density by 11% at 4 months or by 11-17% both at 1 and 4 months of age, respectively. The effect of sound exposure upon neurons expressing the NMDAepsilon1 subunit was dose-dependent. Increasing with age until 4 months in control mice and remaining essentially stable thereafter, the percentage of NMDAepsilon1-immunoreactive neurons was significantly elevated by 40-66% in 1- and 8-month-old SAMP8 exposed to 53 dB, whereas no significant effect of 65 dB was apparent. The proportion of GABAergic cells declined with age in controls. It was significantly decreased at 1 month after 53 and 65 dB sound exposure. In contrast, it was elevated at later stages, being significantly increased at 4 months after exposure to 53 dB and at 8 months after exposure to 65 dB. The total cell number in the 9-kHz isofrequency lamina of SAMP8 decreased with age, but was not affected by exposure to either 53 or 65 dB. The present results indicate that early postnatal exposure to a monotone of mild intensity has long-term effects upon the aging auditory brain stem. Some of the changes induced by sound exposure, e.g., decline in spine density, are interpreted as accelerations of the normal aging process, whereas other effects, e.g., increased NMDAepsilon1 expression after 53 dB and elevated GABA expression after both 53 and 65 dB, are not merely explicable by accelerated aging.

Acoustic Stimulation↗

PubMed2003

A2B5 lineages of human astrocytic tumors and their recurrence.

Astrocytomas are very common intracranial glial cell neoplasms with an inherent tendency to progress. However, the heterogeneity of the morphological features and clinical behavior of the tumors makes accurate prognosis based on the histopathological grading system very difficult. Studies demonstrated that astrocytes have two distinctive cell lineages, and tumors arisen from these two astrocytic lineages have been speculated to have different biological and clinical manifestations. The present study aimed to delineate these two astrocytic lineages in human astrocytomas by using different immunohistochemical markers and to correlate the cell lineages of the tumors with their recurrence. Three markers were used, namely the A2B5 antigen, which is present in type 2 astrocytes but absent in type 1 astrocytes, glial fibrillary acidic protein (GFAP), a marker for astrocytes, and galactocerebroside (GC), a marker for oligodendrocytes. It was found that astrocytomas sharing the A2B5+ lineage (A2B5 positive and GFAP positive) have a significantly higher recurrence rate than the tumors of the A2B5- lineage (A2B5 negative and GFAP positive). Immunohistochemical staining and PCR-single-stranded conformational polymorphism analysis showed that p53 overexpression and p53 mutations were closely associated with the recurrent astrocytomas, and p53 abnormalities were more frequently detected in astrocytomas of the A2B5+ lineage. Quantification of proliferation by counting argyrophil nucleolar organizer regions (AgNORs) indicated a higher AgNOR count in the A2B5+ lineage than the A2B5- lineage. Our findings thus suggest that astrocytomas share similar antigenicity with astrocytes, and that the A2B5+ lineage exhibited a higher recurrence rate than the A2B5- lineage. The higher recurrence rate of the A2B5+ tumors may be in part related to the higher frequency of p53 abnormalities found in the tumors and the higher proliferative activity as reflected by the higher AgNOR count of the tumors.

Antigens, Neoplasm↗

PubMed2002

Proliferation and apoptosis in the developing human neocortex.

The cell kinetics of the developing central nervous system (CNS) is determined by both proliferation and apoptosis. In the human neocortex at week 6 of gestation, proliferation is confined to the ventricular zone, where mitotic figures and nuclear immunoreactivity for proliferating cell nuclear antigen (PCNA) are detectable. Cell division is symmetric, with both daughter cells reentering mitosis. At week 7, the subventricular zone, a secondary proliferative zone, appears. It mainly gives rise to local circuit neurons and glial cells. Around week 12, the ventricular and subventricular zones are thickest, and the nuclear PCNA label is strongest, indicating that proliferation peaks at this stage. Thereafter, asymmetric division becomes the predominant mode of proliferation, with one daughter cell reentering mitosis and the other one migrating out. Towards late gestation, the ventricular and subventricular zones almost completely disappear and proliferation shifts towards the intermediate and subplate zones, where mainly glial cells are generated. A remnant of the subventricular zone with proliferative activity persists into adulthood. In general, proliferation follows a latero-medial gradient in the neocortex lasting longer in its lateral parts. Apoptotic nuclei have been detected around week 5, occurring in low numbers in the ventricular zone at this stage. Apoptotic cell death increases around midgestation and then spreads throughout all cortical layers, with most dying cells located in the ventricular and subventricular zones. This spatial distribution of apoptosis extends into late gestation. During the early postnatal period, most apoptotic cells are still located in the subcortical layers. During early embryonic development, proliferation and apoptosis are closely related, and are probably regulated by common regulators. In the late fetal and early postnatal periods, when proliferation has considerably declined in all cortical layers, apoptosis may occur in neurons whose sprouting axons do not find their targets.

Apoptosis↗

PubMed2002

Pien Tze Huang protects the liver against carbon tetrachloride-induced damage.

Pien Tze Huang, a traditional Chinese medicine, has been extensively used as a therapeutic drug in the treatment of liver diseases. In this study, we have examined its ability to protect the liver from carbon tetrachloride (CCl4)-induced damage in the mouse. Histological observations revealed that CCl4 treatment induced extensive degenerative changes in the hepatocytes surrounding the central veins of the liver. However, these changes were much reduced by more than 28% in mice fed with 0.5 mg of Pien Tze Huang/g body weight/dose (3 doses over 36 hr) prior to CCl4 treatment. The effects of Pien Tze Huang were then further investigated in a hepatoma cell line. Flow analysis showed that it had no significant effects on cell proliferation. When the ability of Pien Tze Huang to influence various response elements of important signal transduction pathways was examined in the hepatoma cell line, it was found that Pien Tze Huang stimulated an increase in the response of AP1, CRE and NFkappaB responsive elements. The transcriptional factors of these responsive elements are known to play important roles in regulating cell death and survival. We thus postulate that the ability of Pien Tze Huang to protect the liver from damage is attained through its ability to modulate the activity of these important signal transduction pathways.

Animals↗

PubMedDate not supplied

Expression of ARVCF in the human ganglionic eminence during fetal development.

ARVCF (armadillo repeat gene deleted in velocardiofacial syndrome) is a recently characterized member of the catenin p120 (ctn) subfamily of the armadillo repeat proteins. It is involved in modulation of cell-cell adhesion essential to many developmental processes including cellular rearrangement and migration. In the present study, by using specific immunohistochemical methods, strongly ARVCF-immunoreactive cells in a high packing density were found in the human ganglionic eminence (GE), a telencephalic structure which gives rise to precursor neurons of the striatum, the amygdala and the basal nucleus of Meynert. From 20 to 25 weeks of gestation, stripes of immunoreactive cells were found to extend from both the superior part of the GE towards the intermediate zone of the neocortex and from the inferior part of the GE either towards the amygdaloid complex or more laterally towards the intermediate zone. Bands of ARVCF-positive cells were also identified in the gangliothalamic body, a transient target for the migrating neurons from the GE to the thalamus. Double immunolabelling with ARVCF and calretinin antibodies, which mark the GE neurons migrating towards the cerebral cortex, revealed that a majority of ARVCF-positive neurons at the periphery of the GE and the cellular extensions from the GE also expressed calretinin. Our results implicate a very close association of ARVCF with migrating neurons from the GE.

Armadillo Domain Proteins↗