PubMed Health⌕ Search

Biomedical subjects

Susumu Higuchi

Publications and source records attributed to Susumu Higuchi.

At least 37 records · Page 2Linked to original sources
PubMed2004

Association between the brain-derived neurotrophic factor 196G/A polymorphism and eating disorders.

Several lines of evidence suggest that genetic factors might contribute to the pathogenesis of eating disorders and that brain-derived neurotrophic factor (BDNF) plays a role in the pathophysiology of eating disorders. To investigate the role of the BDNF gene in the susceptibility to eating disorders, we analyzed the BDNF 196G/A gene polymorphism in female patients with eating disorders and female normal controls. The difference in the genotype frequency between patients (n = 198) and normal controls (n = 222) was statistically significant (P = 0.029). Interestingly, a significant (P = 0.015) difference in the genotype frequency between normal controls and bulimia nervosa patients (n = 101) with binge-purging type was detected. This study suggests that the BDNF 196G/A gene polymorphism might be associated with a susceptibility to eating disorders.

Adolescent↗
PubMed2004

Association of cholecystokinin-A receptor gene polymorphisms and panic disorder in Japanese.

Several lines of evidence have suggested that naturally occurring alterations in cholecystokinin (CCK) systems could contribute to the development of panic disorder (PD). Among recent investigations, polymorphisms of the CCK and CCK-B receptor (R) genes were investigated, but the results were inconclusive. We recently cloned the genomic structures of human CCK-AR, and determined the transcriptional start site of the human CCK-AR gene. Two sequence changes were detected in the promoter region: a G to T change in nucleotide -128 and an A to G change in nucleotide -81 (GenBank database under accession number D85606). The frequencies of the genotypes and haplotypes of these two polymorphisms were compared in 109 Japanese patients with PD and 400 age- and gender-matched normal Japanese control subjects. The frequency of variant genotypes (-81A/G, -128G/T; G/G, G/T, and G/G, T/T) having variant haplotype (-81G/-128T) was significantly higher in PD than in controls (P < 0.0001, OR = 2.81, 95% CI = 1.74-4.39). The statistical differences between the haplotype distributions in the PD and control groups were highly significant: the frequency of variant haplotype (-81G/-128T) was higher in the former group than in the latter (P < 0.0001). This association was not affected by clinical characteristics such as age, gender, and age at onset of PD. In this study, the first to report the positive association of the CCK-AR polymorphisms and PD, haplotype analyses further strengthened the association based on our comparison of genotype distributions. The CCK-AR gene polymorphism may be involved in the neurobiology of PD.

Adolescent↗
PubMed2004

Plasma phosphatidylcholine hydroperoxide as a new marker of oxidative stress in alcoholic patients.

Quantitative analysis of plasma phosphatidylcholine hydroperoxide (PCOOH) is an important step in evaluating the biochemical processes leading to oxidative injury. However, secondary products of lipid peroxidation are now used as indices. One hundred nine alcoholic patients, aged 22-81 years (mean +/- SEM, 52.0 +/- 1.3 years), and 21 healthy volunteers, aged 41-79 years (51.2 +/- 2.2 years), participated in this study. Plasma PCOOH was measured by HPLC with chemiluminescence detection. Plasma PCOOH concentration was significantly higher in alcoholic patients (46.1 +/- 4.1 pmol/ml) than in controls (15.6 +/- 1.8 pmol/ml). It was significantly higher in patients with blood alcohol (88.0 +/- 10.5 pmol/ml) than in those without alcohol (32.6 +/- 3.1 pmol/ml). The patients with high levels of aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transpeptidase (gamma-GTP), and triglyceride (TG) showed significantly higher PCOOH concentrations than did patients with normal levels. The PCOOH level was positively correlated with levels of gamma-GTP, HDL, blood alcohol concentration, and TG. Plasma PCOOH levels in 29 alcoholic patients after a 6 week abstinence were decreased significantly (22.8 +/- 11.1 pmol/ml), which was associated with improvement on liver function tests. This is the first measurement of plasma PCOOH in alcoholic patients. These results suggest the involvement of lipid peroxidation in alcohol-induced liver damage and confirm that the PCOOH plasma concentration is a new marker of alcohol consumption as well as oxidative stress in alcoholic patients.

Adult↗
PubMed2004

Functional polymorphisms in the sigma1 receptor gene associated with alcoholism.

BACKGROUND: Sigma1 receptors are involved in the pathogenesis of drug abuse. Two polymorphisms (GC-241-240TT and Gln2Pro) in the sigma1 receptor gene (SIGMAR1) have been identified. To investigate the role of SIGMAR1 in conveying susceptibility to alcoholism, we performed a functional analysis of polymorphisms in the SIGMAR1 and a case-control study. METHODS: We initially screened for polymorphisms in the 5'-upstream region. The effects of the polymorphisms on transcriptional activity were determined using a gene reporter assay. The distribution of SIGMAR1 polymorphisms was analyzed in 307 alcoholic and 302 control subjects. RESULTS: A novel T-485A polymorphism was identified. The transcriptional activity of the A-485 allele and the TT-241-240 allele was significantly reduced compared with that of the T-485 allele and the GC-241-240 allele. The frequencies of the A-485 allele (chi2=5.575, df=1, p=.0205) and the TT-241-240/Pro2 haplotype (chi2=21.464, df=1, p<.0001) were significantly higher in control subjects compared with alcoholic subjects. The T-485A and the GC-241-240TT may be functional polymorphisms, and the A-485 allele and TT-241-240/Pro2 haplotype are possible protective factors for the development of alcoholism.

Adult↗
PubMed2004

Acetaldehyde accumulation suppresses Kupffer cell release of TNF-Alpha and modifies acute hepatic inflammation in rats.

BACKGROUND: Alcohol-related diseases have multiple and varied associations with acetaldehyde, a highly toxic product of ethanol oxidation that accumulates in the absence of active aldehyde dehydrogenase (ALDH). This study was designed to clarify the role of acetaldehyde in liver injury, specifically in vivo and in vitro effects on Kupffer cell release of the inflammatory cytokine tumor necrosis factor-alpha (TNF-Alpha). METHODS: Rats pretreated overnight with the ALDH inhibitor disulfiram (or saline control) were ethanol loaded and challenged with lipopolysaccharide (LPS), and their blood and histological parameters were examined 3 h later. Similarly, isolated rat Kupffer cells were pretreated with disulfiram or cyanamide incubated in ethanol (1 h), then challenged with LPS and evaluated 2 h later for TNF-Alpha and acetaldehyde levels in the culture medium. TNF-Alpha release from Kupffer cells after LPS challenge was also evaluated following incubation in acetaldehyde and acetate for comparison with ethanol loading. RESULTS: Higher blood acetaldehyde concentration following disulfiram pretreatment significantly attenuated acute hepatic inflammation in the ethanol-loaded, LPS-challenged rat (18 +/- 2.9 vs 30 +/- 3.7 polymorphonuclear cells/portal area; P = 0.01). After LPS challenge, ALDH inhibitor pretreatment attenuated Kupffer cell release of TNF-Alpha in the presence of disulfiram at 5063 +/- 151 pg/ml and cyanamide at 4390 +/- 934 pg/ml, versus no inhibitor, 5869 +/- 265 pg/ml ( P < 0.01), but not in the absence of ethanol. Acetaldehyde significantly suppressed Kupffer cell TNF-Alpha release ( P < 0.05), but acetate treatment did not. CONCLUSIONS: Acetaldehyde accumulation suppresses macrophage function, at least suppressing TNF-Alpha release, which plays a role in modifying acute hepatic inflammation in rats.

Acetaldehyde↗
PubMed2004

Severe chronic pancreatitis and severe liver cirrhosis have different frequencies and are independent risk factors in male Japanese alcoholics.

BACKGROUND: Chronic pancreatitis and liver cirrhosis are major alcohol-related diseases in most countries. Neither their specific etiologies nor the relationship between them is fully understood. This study was designed to examine a possible association between alcoholic chronic pancreatitis (ACP) and alcoholic liver cirrhosis (ALC), and to identify factors relating to them. METHODS: The subjects were 141 consenting participants from 1087 male patients consecutively admitted to Kurihama National Hospital from July 2000 to November 2002. All were negative for major medical disorders (e.g., viral hepatitis, operative history, malignancy), except for ACP and ALC. Analysis of each subject included background information (collected by face-to-face interview, regarding quantity and duration of drinking, usual alcoholic drinks, smoking, education, employment, and marital status) and signs of ACP detected on endoscopic retrograde cholangiopancreatography (ERCP) and ALC indicated by Child-Pugh classification. Subjects consenting to genome analyses ( n = 83) were genotyped for two key alcohol-metabolizing enzymes: alcohol dehydrogenase-2 and aldehyde dehydrogenase-2. RESULTS: Grouping patients by ERCP grading and Child classification revealed a nonparallel relationship between the severities of the two diseases. This relationship held, even after controlling for several pertinent background variables (sociofamilial, drinking, clinical, and genetic factors) by logistic regression analysis. The drinking of spirits and a high daily consumption of alcohol were independent risk factors for ACP, while never-married status was the only risk factor identified with ALC among these male Japanese patients. CONCLUSIONS: Different risk factors may confer susceptibility to ACP versus ALC, which may explain the nonparallel relationship between the severities of the two diseases in Japanese alcoholics.

Adult↗
PubMed2004

Prolonged central sensory conduction time in alcoholics with hypoactive aldehyde dehydrogenase-2.

People who have a Glu487Lys mutation (single nucleotide polymorphism) in the aldehyde dehydrogenase-2 (ALDH2) gene are slow to metabolize the alcohol breakdown product acetaldehyde. The P13/14-N20 interval of the median nerve somatosensory evoked potential was significantly longer in alcoholic patients with a hypoactive ALDH2 (n = 27) than in those with an active ALDH2 (n = 43). This suggests that acetaldehyde accumulation due to hypoactive ALDH2 is associated with a prolongation of the central sensory conduction time between pons and primary sensory cortex. The present result indicates that an elevated blood concentration of acetaldehyde must cause the central sensory tract involvement and that acetaldehyde is one of factors producing brain damage in alcoholics.

Acetaldehyde↗
PubMed2004

ALDH2/ADH2 polymorphism associated with vasculopathy and neuropathy in type 2 diabetes.

In the history of diabetes, chlorpropamide alcohol flushing test (CPAF) was a big topic in the 1970s to 1980s. Alcohol tolerance after chlorpropamide has prognostic significance, with the intolerant group (CPAF-positive group) being less prone to develop vascular complication than the tolerant group (CPAF-negative group). A mechanism of CPAF has been regarded as the inhibition of aldehyde dehydrogenase 2 (ALDH2) by an N-alkyl-substituted derivative of chlorpropamide, and the expression of these mutations of ALDH2 and alcohol dehydrogenase 2 (ADH2) could determine the alcohol tolerance among the Japanese population. Therefore, we hypothesized that expression of different ALDH2 and ADH2 polymorphisms may induce differences in vascular complications in diabetes and conducted two studies. The first study (study 1) was to determine the association of ALDH2/AHD2 polymorphism with diabetic complications. To know the association of ALDH2/AHD2 polymorphism with diabetic vasculopathy and neuropathy, a total of 158 patients with type 2 diabetes were divided into four groups on the basis of ALDH2 "activity" and ADH2 "superactivity." The frequency of proteinuria and the percentage of proliferative retinopathy among the patients with retinopathy was higher in those with active ALDH2 and superactive ADH2. We speculated that protein kinase C isoforms up-regulated by 4-hydroxynonenal that was detoxified by ALDH2 and ADH2 may account for the long-term development of diabetic nephropathy and severe retinopathy. As for neuropathy, the frequency of symptomatic neuropathy was higher in patients with inactive ALDH2 and usual ADH2. We speculate that increased tissue levels of toxic aldehyde could result from inactive ALDH2 and usual ADH2 expression, which results in the increased level of reactive aldehyde in sensory neuron pathway, thereby causing symptomatic polyneuropathy.

Adolescent↗
PubMed2004

Association study of brain-derived neurotrophic factor gene polymorphism and alcoholism.

OBJECTIVE: Brain-derived neurotrophic factor (BDNF) influences dopamine and serotonin neurotransmitters that are heavily linked to addiction. A quantitative trait loci study indicated that genes localized to 11p13, where the BDNF gene is mapped (11p13-15), increase the risk for severe alcohol withdrawal. Moreover, a recent study using a pooled-sample microarray suggested that the BDNF gene locus was included in the loci that were shown to be associated with drug abuse. These lines of evidence suggested that BDNF might play some role in the development of or vulnerability to alcoholism and/or clinical characteristics of alcoholic individuals. METHODS: The alcoholic subjects consisted of 377 male Japanese patients. A structured interview was used to obtain social background, drinking history, history of violence while intoxicated, history of alcohol withdrawal, and family history of alcoholism. The control group consisted of 336 nonalcoholic male subjects. Genotyping of the G196A polymorphism of the BDNF gene was done by polymerase chain reaction (PCR)-restriction fragment length polymorphism method. RESULTS: Genotype and allele distributions of the BDNF gene polymorphism did not differ significantly between alcoholic and control subjects. However, comparing clinical characteristics across G196A genotypes, we found that alcoholic subjects with violent tendencies and a history of delirium tremens had a significantly higher frequency of AA genotypes and A allele frequencies than those without them. Moreover, alcoholic subjects with the A allele had earlier onset of the disease than those without it. CONCLUSIONS: These results indicate that BDNF gene polymorphism might modify phenotypes of alcoholism.

Alcoholism↗
PubMed2004

The Japanese society of alcohol-related problems.

This paper presents an outline of the Japanese Society of Alcohol-Related Problems. The precursor of the Society was the Japan Alcoholism Treatment Research Group, inaugurated in 1979, by merging two local research groups in the Tokyo and Osaka areas, both of which were exclusive gatherings of psychiatrists associated with alcoholism clinics. The Research Group developed into the Society in 1992, as the number of participants including those from other medical professions increased yearly, and the subjects of the group widened to include all addictive behaviours. In reflecting the process of establishment, it is unique in many aspects as a scientific society. The Society is not a science-orientated body for presentation of new research findings. The main programme of the annual meeting is therefore a set of symposia in which members participate and discuss clinical and/or social problems arising from dependency on alcohol or drugs. Perhaps because of its content, the annual meeting is attended each year by the largest number of participants among all the societies in Japan concerned with alcohol and drugs. For the next several years, the Society's activities will be directed at (1) establishment of guidelines for early identification of and intervention in alcohol-related problems; (2) expansion of its membership to include those in related fields of medicine and non-medical professions; (3) improvement of the system of journal publication; and (4) creation of a system for timely adequate response to social problems associated with drugs and alcohol.

Alcohol-Related Disorders↗
PubMed2004

Influence of genetic variations of ethanol-metabolizing enzymes on phenotypes of alcohol-related disorders.

Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase-2 (ALDH2) play central roles in the metabolism of ethanol and its metabolite, acetaldehyde, in the liver. In ADH2, one nucleotide replacement causes either a super-active beta 2 subunit encoded by the ADH2*2 allele or a less active beta 1 subunit (ADH2*1 allele). In the same way, a G/A replacement at codon 487 of the ALDH2 gene produces an inactive form of the enzyme. Because the geno-types of these genes may explain individual differences in concentration and elimination of ethanol and acetaldehyde in the blood after drinking, they could be used as models to elucidate the contribution of these substances to the development of addiction and various types of organ damage. We have examined the influence of genetic variations of these enzymes on alcohol-related disorders in the Japanese. The results revealed that (1) the less active allele of the ADH2 gene (ADH2*1) is associated with an increased risk for alcohol dependence, alcohol-induced persistent amnestic disorder, alcohol withdrawal syndrome, and cancer of the upper GI tract; (2) the inactive allele of the ALDH2 gene (ALDH2*2) is associated with a decreased risk for alcohol dependence, and an increased risk for alcoholic polyneuropathy and cancer in the same region; and (3) these genetic variations modify clinical features of alcohol dependence. Possible mechanisms of altered risk for these disorders are discussed.

Alcohol Dehydrogenase↗
PubMed2004

Homozygous (TG)11 allele in intron 8 of the cystic fibrosis transmembrane conductance regulator (CFTR) gene has a protective role against bicarbonate decrease in pure pancreatic juice among Japanese male alcoholics.

BACKGROUND: Heavy drinkers have a high incidence of chronic pancreatitis (CP), but the mechanism of alcohol-related CP is largely unknown. Exocrine pancreatic insufficiency exists in about 90% of the patients with cystic fibrosis (CF), which results from an abnormal cystic fibrosis transmembrane conductance regulator gene (CFTR). AIM: To investigate in Japanese alcoholics the association between bicarbonate concentration in pure pancreatic juice and one of the polymorphisms of the CFTR gene, the (TG)m Tn tract length in intron 8. METHODS: Fifty-six patients under treatment for alcohol dependence were stimulated by intravenous injection of secretin during endoscopic retrograde cholangiopancreatography to provide pancreatic juice specimens. Individual maximum bicarbonate concentrations (MBC) were compared with (TG)m Tn tract polymorphisms identified by directly sequencing lymphocyte DNA. RESULTS: Among the 41 patients able to provide adequate pancreatic juice specimens, 15 had low MBC and 26 had normal MBC. The frequencies of the six haplotypes identified in these patients were 17.1% (TG)11T7/(TG)llT7, 46.3% (TG)11T7/(TG)12T7, 29.3% (TG)12T7/(TG)12T7, 2.4% (TG)10T9/(TG)11T7, 2.4% (TG)12T5/(TG)11T7, and 2.4% (TG)12T6/(TG)12T7. Among the 92.7% of patients who had the common (TG) miT7/(TG)m2T7 haplotype, all of the 7 with homozygous (TG)11 alleles had normal MBC (p<0.05). CONCLUSION: Alcoholics with homozygous (TG)11 alleles in intron 8 of the CFTR gene appear to be protected against decreased MBC, compared with those who have the (TG)11/(TG)12 and (TG)12/(TG)12 genotypes, suggesting a role for CFTR gene polymorphism in the progression of alcohol-related pancreatic disease.

Adult↗
PubMed2004

[Introduction of cognitive-behavioral therapy for alcoholic inpatients at Kurihama National Hospital].

A new inpatient treatment program for alcoholism based on cognitive-behavioral therapy was introduced at Kurihama National Hospital in March 2000. We have classified the dysfunctional cognitions frequently exhibited by alcoholics into eight categories. The therapy is premised on the notion that the presence of one or more of the dysfunctional cognitions can trigger worsening of an alcoholic's drinking problem. We have devised a cognitive model in which the patients themselves examine their dysfunctional cognitions and recover from the vicious cycle of alcoholism. Cognitive-behavioral therapy is conducted at Kurihama National Hospital based on these hypotheses. The cognitive-behavioral therapy employed at Kurihama National Hospital is administered in group therapy in an inpatient treatment setting. Since the treatment is provided on an inpatient basis, dropouts from the program as a result of the patient starting to drink again can be prevented. Furthermore, since group therapy are used, cognitions of alcohol are examined not just in the context of the relationship between patient and therapist, but also in the context of the relationships among patients. It thus becomes easier to examine dysfunctional cognitions from a multifaceted perspective. It will be easier for patients to examine their future drinking behavior concretely through the introduction of cognitive-behavioral therapy, and improvements in outcome should be achieved. However, the relationship between change in cognitions and prognosis needs to be studied in the future.

Alcohol Drinking↗
PubMed2004

[Diagnosing the mild cognitive impairment stage of Alzheimer's disease].

Recently, it has become important to diagnose Alzheimer's Disease (AD) at an early stage due to the development of AD therapy. Also, there is increasing recognition of a class of elderly people with complaints of memory loss but who nevertheless do not meet the criteria for dementia. "Mild cognitive impairment" (MCI) is the term used for this disorder, and amnestic MCI is highly converted to AD. In this study we evaluated the accuracy of diagnosis of amnestic MCI by cerebrospinal fluid total-tau protein (CSF/total-tau), cerebrospinal fluid amyloid beta 1-42 protein (CSF/A beta 1-42), and cerebral blood flow in the posterior cingulate cortex using SPECT. CSF/total-tau was the most appropriate to discriminate between normal cognitive individuals and those with amnestic MCI. We also evaluated the CSF/total-tau and MRI images between patients with stable MCI and those with progressive MCI, including those who converted to AD in the following two years. The stable type was characterized by normal CSF/total-tau levels and relatively high grade periventricular white matter lesions (PWML). Conversely, the progressive type was characterized by high CSF-tau levels and relatively low grade PWML. We speculate that stable MCI is due to ischemic change with in the white matter lesion, while progressive MCI may represent a previous stage of AD.

Alzheimer Disease↗
PubMed2003

Macrocytosis, a new predictor for esophageal squamous cell carcinoma in Japanese alcoholic men.

Early esophageal squamous cell carcinoma detected by esophageal iodine staining can be easily treated by endoscopic mucosectomy, and identifying its predictors is important in better selecting candidates to screen for this high-mortality cancer. The common etiologies of elevated mean corpuscular volume (MCV) and esophageal cancer, including folate deficiency, smoking, drinking and high acetaldehyde exposure, suggest testing MCV as such a predictor. Japanese alcoholic men with (n = 65) and without (n = 206) esophageal squamous cell carcinomas, excluding those with liver cirrhosis, were assessed for MCV within 7 days of their last drink, alone or in combination with findings from either the alcohol flushing questionnaire or genotyping to identify inactive aldehyde dehydrogenase-2 (ALDH2*1/2*2) and the less-active form of alcohol dehydrogenase-2 (ADH2*1/2*1), which pose risks for esophageal squamous cell carcinoma. MCV was higher in cancer patients than in the control group. MCV was higher in both groups in those who were heavier smokers, had lower body mass index (BMI), experienced alcohol flushing, and had ALDH2*1/2*2. After adjusting for age, drinking and smoking habits, BMI and ALDH2/ADH2 genotypes, macrocytosis of MCV > or =106 fl was associated with increased risk for esophageal cancer (OR = 2.75). Men with both MCV > or =106 fl and alcohol flushing had an even higher cancer risk (OR = 5.51). The combinations of MCV > or =106 fl with ALDH2*1/2*2 or ADH2*1/2*1 alone, and both ALDH2*1/2*2 and ADH2*1/2*1 (ORs = 11.44, 21.22 and 319.7, respectively) showed consistently higher risk than the corresponding group with MCV <106 fl (ORs = 7.24, 4.71 and 27.01, respectively). In conclusion, MCV measurement, alone or in combination with the markers of alcohol sensitivity, provides a new means of predicting risk for esophageal squamous cell carcinoma in Japanese alcoholic men.

Alcohol Dehydrogenase↗
PubMed2003

Benign type of central pontine myelinolysis in alcoholism--clinical, neuroradiological and electrophysiological findings.

Nine alcoholic patients with central pontine myelinolysis (CPM),who showed a favorable prognosis, are reported. The majority of them had taken part in binge drinking and had a subsequent consciousness disturbance for 18.1+/-10.9 (mean+/-SD) days. None of the patients had had acute correction of hyponatremia. Truncal ataxia and gait instability were present in most of the patients after recovery from the disturbance of consciousness. Most of them eventually gained independence, and magnetic resonance imaging showed that their pontine lesions tended to shrink. Electrophysiological studies detected prolonged latency between the I and III waves in auditory brainstem responses and between N11 and P13/14 onsets in the somatosensory evoked potentials. These clinical, radiological and electrophysiological findings should be of use in diagnosing CPM.

Adult↗
PubMed2003

Association of dystroglycan and laminin-2 coexpression with myelinogenesis in peripheral nerves.

To provide clues to the biological functions of dystroglycan-laminin-2 complex in peripheral nerves, we investigated the expressions of beta-dystroglycan and laminin-alpha(2) chain in rat sciatic nerve during axonal degeneration and regeneration and during development, as well as in rat dorsal root ganglia. In normal conditions, immunoreactivity of the cytoplasmic domain of beta-dystroglycan was associated with the Schwann cell abaxonal membrane. The immunoreactivities of both beta-dystroglycan and the laminin-alpha(2) chain decreased in Schwann cells losing axons during axonal degeneration and progressively increased in remyelinating Schwann cells during axonal regeneration. Interestingly, during axonal degeneration, the abaxonal membrane losing contact with the basal lamina lost the association with beta-dystroglycan immunoreactivity. During development, expression of both beta-dystroglycan and laminin-alpha(2) chain strikingly increased during postnatal 7 days, which is a critical period when basal lamina assembly and myelin formation rapidly progress. These results suggest that coexpression of dystroglycan and laminin-2 is associated with myelinogenesis in peripheral nerves. These two proteins may function as an anchorage between the abaxonal membrane and the basal lamina, enabling myelin forma-tion to progress. Beta-dystroglycan and laminin-2 were also coexpressed in satellite cells in dorsal root ganglia, suggesting that interaction of these two proteins plays some role in physiological functions of these cells.

Animals↗