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1.
Febrile seizures (FS) are common in children, and the incidence is 2–5% before the age of 5 years. A four-generation Chinese
family with autosomal dominant febrile seizure and epilepsy was studied by genome-wide linkage analysis. Significant linkage
was identified with markers on chromosome 3q26.2–26.33 with a maximum pairwise LOD score of >3.00. Fine mapping defined the
new genetic locus within a 10.7-Mb region between markers D3S3656 and D3S1232. A maximum multipoint LOD score of 5.27 was detected at marker D3S1565. A previously reported CLCN2 gene for epilepsy was excluded as the disease-causing gene in the family by mutational analysis of all exons and exon–intron
boundaries of CLCN2 and by haplotype analysis. Mutation analysis of KCNMB2 and KCNMB3, which were two potassium-channel genes in this linkage region, did not reveal a disease causing mutation. Our results identified
another novel locus on chromosome 3q26.2–26.33, and future studies of the candidate genes at the locus will identify a new
gene for combined FS and idiopathic epilepsies.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
X.-H. Dai, W.-W. Chen, and X. Wang contributed equally to this work. 相似文献
2.
Rinki Ratnapriya Joseph Vijai Jayaram S. Kadandale Rajesh S. Iyer Kurupath Radhakrishnan Anuranjan Anand 《Human genetics》2010,128(2):123-130
We performed a whole genome linkage analysis in a three-generation south Indian family with multiple members affected with
juvenile myoclonic epilepsy (JME). The maximum two-point LOD score obtained was 3.32 at recombination fraction (θ) = 0 for
D2S2248. The highest multipoint score of 3.59 was observed for the genomic interval between D2S2322 and D2S2228 at the chromosomal
region 2q33–q36. Proximal and distal boundaries of the critical genetic interval were defined by D2S116 and D2S2390, respectively.
A 24-Mb haplotype was found to co-segregate with JME in the family. While any potentially causative variant in the functional
candidate genes, SLC4A3, SLC23A3, SLC11A1 and KCNE4, was not detected, we propose to examine brain-expressed NRP2, MAP2, PAX3, GPR1, TNS1 and DNPEP, and other such positional candidate genes to identify the disease-causing gene for the disorder. 相似文献
3.
Arun Kumar Maheswara R. Duvvari Venkatesh C. Prabhakaran Jyoti S. Shetty Gowri J. Murthy Susan H. Blanton 《Human genetics》2010,128(4):365-371
Microspherophakia is an autosomal-recessive congenital disorder characterized by small spherical lens. It may be isolated
or occur as part of a hereditary systemic disorder, such as Marfan syndrome, autosomal dominant and recessive forms of Weill-Marchesani
syndrome, autosomal dominant glaucoma–lens ectopia–microspherophakia–stiffness–shortness syndrome, autosomal dominant microspherophakia
with hernia, and microspherophakia-metaphyseal dysplasia. The purpose of this study was to map and identify the gene for isolated
microspherophakia in two consanguineous Indian families. Using a whole-genome linkage scan in one family, we identified a
likely locus for microspherophakia (MSP1) on chromosome 14q24.1–q32.12 between markers D14S588 and D14S1050 in a physical
distance of 22.76 Mb. The maximum multi-point lod score was 2.91 between markers D14S1020 and D14S606. The MSP1 candidate
region harbors 110 reference genes. DNA sequence analysis of one of the genes, LTBP2, detected a homozygous duplication (insertion) mutation, c.5446dupC, in the last exon (exon 36) in affected family members.
This homozygous mutation is predicted to elongate the LTBP2 protein by replacing the last 6 amino acids with 27 novel amino
acids. Microspherophakia in the second family did not map to this locus, suggesting genetic heterogeneity. The present study
suggests a role for LTBP2 in the structural stability of ciliary zonules, and growth and development of lens. 相似文献
4.
Juvenile myoclonic epilepsy is a clinically well-defined, age-related common idiopathic generalized epilepsy syndrome with
substantial genetic basis to its etiology. We report identification of a novel epilepsy locus at chromosome 5q12–q14 in a
family exhibiting autosomal dominant form of juvenile myoclonic epilepsy from south India. The highest two-point LOD score
of 3.3344 was obtained for the microsatellite markers D5S641 and D5S459 at 5q14. Centromeric and telomeric chromosomal boundaries
of the locus were defined by D5S624 and D5S428, respectively. The 5q12–q14 locus encompasses about 25 megabases of the genomic
region and harbours several candidate genes. Further work involving a detailed mutational analysis of the locus, to isolate
the gene responsible for the epilepsy disorder in the family, shall help enhance our understanding of molecular basis of epilepsy
disorders. 相似文献
5.
Alopecia with mental retardation syndrome is a rare autosomal recessive disorder characterized clinically by total or partial
alopecia and mental retardation. In an effort to understand the molecular bases of this form of alopecia syndrome, large Pakistani
consanguineous kindred with multiple affected individuals has been ascertained from a remote region in Pakistan. Genome wide
scan mapped the disease locus on chromosome 3q26.33–q27.3. A maximum two-point LOD score of 3.05 (θ=0.0) was obtained at marker
D3S3583. Maximum multipoint LOD score exceeding 5.0, obtained with several markers, supported the linkage. Recombination events
observed in affected individuals localized the disease locus between markers D3S1232 and D3S2436, spanning 11.49-cM region
on chromosome 3q26.33–q27.3. Sequence analysis of a candidate gene ETS variant gene 5 from DNA samples of two affected individuals
of the family revealed no mutation. 相似文献
6.
Singh RK Indra D Mitra S Mondal RK Basu PS Roy A Roychowdhury S Panda CK 《Human genetics》2007,122(1):71-81
The aim of this study was to locate the candidate tumor suppressor genes (TSGs) loci in the chromosomal 4p15-16, 4q22-23 and
4q34-35 regions associated with the development of uterine cervical carcinoma (CA-CX). Deletion mapping of the regions by
microsatellite markers identified six discrete areas with high frequency of deletions, viz. 4p16.2 (D1: 40%), 4p15.31 (D2:
35–38%), 4p15.2 (D3: 37–40%), 4q22.2 (D4: 34%), 4q34.2-34.3 (D5: 37–59%) and 4q35.1 (D6: 40–50%). Significant correlation
was noted among the deleted regions D1, D2 and D3. The deletions in D1, D2, D5 and D6 regions are suggested to be associated
with the cervical intraepithelial neoplasia (CIN), and deletions in the D2, D3, D5 and D6 regions seems to be associated with
progression of CA-CX. The deletions in the D2 and D6 regions showed significant prognostic implications (P = 0.001; 0.02). The expression of the candidate TSG SLIT2 mapped to D2 region gradually reduced from normal cervix uteri
→CIN → CA-CX. SLIT2 promoter hypermethylation was seen in 28% CIN samples and significantly increased with tumor progression
(P = 0.04). Significant correlation was seen between SLIT2 deletion and its promoter methylation (P = 0.001), indicating that both these phenomena could occur simultaneously to inactivate this gene. Immunohistochemical analysis
showed reduced expression of SLIT2 in cervical lesions and CA-CX cell lines. Although no mutation was detected in the SLIT2
promoter region (−432 to + 55 bp), CC and AA haplotypes were seen in −227 and −195 positions, respectively. Thus, it indicates
that inactivation of SLIT2-ROBO1 signaling pathway may have an important role in CA-CX development. 相似文献
7.
W. H. Raskind Tamara Bolin John Wolff John Fink Mark Matsushita Michael Litt Hillary Lipe Thomas D. Bird 《Human genetics》1998,102(1):93-97
Paroxysmal dystonic choreoathetosis (PDC) is a rare neurological disorder characterized by episodes of involuntary movement,
involving the extremities and face, which may occur spontaneously or be precipitated by caffeine, alcohol, anxiety, and fatigue.
PDC is transmitted as an autosomal dominant trait with incomplete penetrance. A gene implicated in this paroxysmal disorder
has been mapped to a 10–15 cM region on chromosome 2q31–36 in two families. We describe a third family with PDC. Two-point
linkage analyses with markers linked to the candidate PDC locus were performed. A maximum two-point LOD score of 4.20 at a
recombination fraction of zero was obtained for marker D2S120, confirming linkage to the distal portion of chromosome 2q.
The anion exchanger gene, SLC2C, maps to this region, but the family was poorly informative for polymorphic markers within
and flanking this candidate gene. Haplotype analysis revealed a critical recombination event that confines the PDC gene to
a 5-cM region bounded by the markers D2S164 and D2S377. We compared the haplotype in our family with that in another chromosome
2-linked PDC family, but did not detect a region of shared genotypes. However, identifying a third family whose disease maps
to the same region and narrowing the critical region will facilitate identification of the 2q-linked PDC gene.
Received: 10 June 1997 / Accepted: 17 September 1997 相似文献
8.
Kate V. Everett Barry A. Chioza Christina Georgoula Ashley Reece R. Mark Gardiner Eddie M. K. Chung 《Human genetics》2009,126(6):819-831
Infantile hypertrophic pyloric stenosis (IHPS) is the most common inherited form of gastrointestinal obstruction in infancy
with a striking male preponderance. Infants present with vomiting due to gastric outlet obstruction caused by hypertrophy
of the smooth muscle of the pylorus. Two loci specific to extended pedigrees displaying autosomal dominant inheritance have
been identified. A genome scan identified loci on chromosomes 11q14–q22 and Xq23–q24 which are predicted to be responsible
for a subset of smaller families with IHPS demonstrating non-Mendelian inheritance. The two linked chromosomal regions both
harbour functional candidate genes which are members of the canonical transient receptor potential (TRPC) family of ion channels.
Both TRPC5 (Xq23–q24) and TRPC6 (11q14–q22) have a potential role in smooth muscle control and hypertrophy. Here, we report suggestive evidence for a third
locus on chromosome 3q12–q25 (Z
max = 2.7, p < 0.004), a region which harbours a third TRPC gene, TRPC1. Fine mapping of all three genes using a tagSNP approach and re-sequencing identified a SNP in the promoter region of TRPC6 and a missense variant in exon 4 of TRPC6 which may be putative causal variants. 相似文献
9.
Liu P Zhang S Yao Q Liu X Wang X Huang C Huang X Wang P Yuan M Liu JY Wang QK Liu M 《Human genetics》2008,124(5):507-513
Disseminated superficial actinic porokeratosis (DSAP) is a chronic autosomal dominant cutaneous disorder with high genetic
heterogeneity. Two genetic loci for DSAP were identified, but no specific genes were reported to date. The pathogenic mechanism
of this disorder remains to be elucidated. In this study, a large, five-generation Chinese family with DSAP was genetically
characterized. Two known DSAP loci, DSAP1 and DSAP2, two DSAP candidate genes (SART3 and SSH1), one DSP-linked locus and one PPPD-linked locus were first excluded in the family. The family was then characterized by
genome-wide linkage analysis and a new DSAP locus was identified on chromosome 1p31.3–p31.1 with a maximum two-point LOD score
of 5.09 with marker D1S2897 (θ = 0). Fine mapping showed that the disease gene was located within an 8.2 cM or 11.9 Mb region between markers D1S438 and D1S464. This is the third locus identified for DSAP (DSAP3). Eight candidate genes including GNG12, IL12RB2, ITGB3BP, DNAJ6, PIN1L, GADD45A, RPE65 and NEGR1 were sequenced, but found to be negative for functional sequence variants. Further mutational analysis of the candidate genes
in the region will identify the specific gene for DSAP, which will provide insights into the pathogenesis of DSAP. 相似文献
10.
A new locus for autosomal dominant Charcot-Marie-Tooth disease type 2 (CMT2L) maps to chromosome 12q24 总被引:12,自引:0,他引:12
Tang BS Luo W Xia K Xiao JF Jiang H Shen L Tang JG Zhao GH Cai F Pan Q Dai HP Yang QD Xia JH Evgrafov OV 《Human genetics》2004,114(6):527-533
Charcot-Marie-Tooth disease (CMT) is one of the most common inherited neurological disorders with a prevalence estimated at 1/2500. The axonal form of this disorder is referred to as Charcot-Marie-Tooth type 2 disease (CMT2). Recently, a large Chinese family with CMT2 was found in the Hunan and Hubei provinces of China. The known loci for CMT1A, CMT2D, CMT1B (the same locus is also responsible for CMT2I and CMT2J), CMT2A, CMT2E, and CMT2F were excluded in this family by linkage analysis. A genome-wide screening was then carried out, and the results revealed linkage of CMT2 to a locus at chromosome 12q24. Haplotype construction and analyses localized this novel locus to a 6.8-cM interval between microsatellite markers D12S366 and D12S1611. The maximal two-point LOD score of 6.35 and multipoint LOD score of 8.08 for marker D12S76 at a recombination fraction () of 0 strongly supported linkage to this locus. Thus, CMT2 neuropathy in this family represents a novel genetic entity that we have designated as CMT2L. 相似文献
11.
We report a consanguineous Pakistani family with seven affected individuals showing a syndromic form of congenital microcephaly.
Clinical features of affected individuals include congenital microcephaly with sharply slopping forehead, moderate to severe
mental retardation, anonychia congenita, and digital malformations. By screening human genome with microsatellite markers,
this autosomal recessive condition was mapped to a 25.2 cM interval between markers D18S1150 and D18S1100 on chromosome 18p11.22–q12.3.
However, the region of continuous homozygosity between markers D18S1150 and D18S997 spanning 15.33 cM, probably define the
most likely candidate region for this condition. This region encompasses a physical distance of 12.03 Mb. The highest two-point
LOD score of 3.03 was obtained with a marker D18S1104 and multipoint score reached a maximum of 3.43 with several markers.
Six candidate genes, CEP76, ESCO1, SEH1L, TUBB6, ZNF519, and PTPN2 were sequenced, and were found to be negative for functional sequence variants. 相似文献
12.
Deprez L Claes LR Claeys KG Audenaert D Van Dyck T Goossens D Van Paesschen W Del-Favero J Van Broeckhoven C De Jonghe P 《Human genetics》2006,118(5):618-625
Febrile seizures (FS) represent the most common seizure disorder in childhood and contribution of a genetic predisposition
has been clearly proven. In some families FS is associated with a wide variety of afebrile seizures. Generalized epilepsy
with febrile seizures plus (GEFS+) is a familial epilepsy syndrome with a spectrum of phenotypes including FS, atypical febrile
seizures (FS+) and afebrile generalized and partial seizures. Mutations in the genes SCN1B, SCN1A and GABRG2 were identified in GEFS+ families. GEFS+ is genetically heterogeneous and mutations in these three genes were detected in
only a minority of the families. We performed a 10 cM density genome-wide scan in a multigenerational family with febrile
seizures and epilepsy and obtained a maximal multipoint LOD score of 3.12 with markers on chromosome 5q14.3-q23.1. Fine mapping
and segregation analysis defined a genetic interval of ≈33 cM between D5S2103 and D5S1975. This candidate region overlapped
with a previously reported locus for febrile seizures (FEB4) in the Japanese population, in which MASS1 was proposed as disease gene. Mutation analysis of the exons and exon–intron boundaries of MASS1 in our family did not reveal a disease causing mutation. Our linkage data confirm for the first time that a locus on chromosome
5q14-q23 plays a role in idiopathic epilepsies. However, our mutation data is negative and do not support a role for MASS1 suggesting that another gene within or near the FEB4 locus might exist. 相似文献
13.
Linkage analysis was performed on a large Danish family to refine the position of RP18, the locus for autosomal dominant retinitis
pigmentosa, mapped previously between D1S534 and D1S305 in chromosome 1p13–q21. We genotyped the family members for five microsatellite-type
DNA polymorphisms and mapped RP18 between D1S422 and D1S2858 to a region of less than 2 cM. No obvious candidate gene has
yet been assigned to the chromosomal interval defined here.
Received: 15 September 1997 / Accepted: 12 January 1998 相似文献
14.
Gul Naz Ghazanfar Ali Syed Kamran-ul-Hassan Naqvi Zahid Azeem Wasim Ahmad 《Human genetics》2010,127(4):395-401
Autosomal recessive hypotrichosis is a rare form of human genetic disorder characterized by sparse to absent hair on scalp
and rest of the body of affected individuals. Over the past few years at least five autosomal recessive forms of hypotrichosis
loci have been mapped on different human chromosomes. In the present study, we report localization of another novel autosomal
recessive hypotrichosis locus on human chromosome 10q11.23–22.3 in a four generation consanguineous Pakistani family. All
the four patients in the family showed typical features of hereditary hypotrichosis including sparse hair on the scalp and
rest of the body. Human genome scan using highly polymorphic microsatellite markers mapped the disease locus to a large region
on chromosome 10. This novel locus maps to 29.81 cM (28.5 Mb) region, flanked by markers D10S538 and D10S2327 on chromosome
10q11.23–22.3. A maximum multipoint LOD score of 3.26 was obtained with several markers in this region. DNA sequence analysis
of exons and splice-junction sites of four putative candidate genes (P4HA1, ZNF365, ZMYND17, MYST4), located in the linkage interval, were sequenced but were negative for functional sequence variants. 相似文献
15.
Isolated autosomal dominant hypoparathyroidism is a heterogeneous disorder characterized by parathyroid hormone (PTH) deficiency,
hypocalcemia and hyperphosphatemia. The candidate gene approach was used to study a large Norwegian family. The loci for the
PTH gene, PTH receptor gene and RET protooncogene were excluded using dinucleotide markers and restriction fragment length
polymorphism analysis. Complete cosegregation of this trait was found with the chromosomal region 3q13, using the short tandem
repeat markers D3S1267, D3S1269, D3S1303, D3S1518, and RHO. This region contains the candidate locus for the Ca2+-sensing receptor (PCAR1). By single-strand conformation polymorphism (SSCP) analysis of all PCAR1 exons followed by automated
sequencing, we identified a C to T transition in exon 2 (cDNA position 452) on the mutant allele in the family. The mutation
predicts a substitution of Thr to Met in amino acid position 151 (T151M). A StyI restriction site created by the nucleotide substitution was used to confirm the mutation on all alleles, as well as to exclude
it among 100 normal alleles (blood donors). SSCP analysis also identified a novel polymorphism of PCAR1 intron 4 (1609–88t→c)
on normal alleles.The T151M mutation is located in the extracellular N-terminal domain of PCAR1, which belongs to the superfamily
of G protein-coupled receptors. We suggest that this is a gain-of-function mutation that increases the sensitivity of the
receptor to [Ca2+], thereby decreasing the calcium set point.
Received: 29 September 1995 / Revised: 19 January 1996 相似文献
16.
Rinki Ratnapriya Parthasarthy Satishchandra S. Dilip Girish Gadre Anuranjan Anand 《Human genetics》2009,126(5):677-683
Hot water epilepsy is a reflex or sensory epilepsy in which seizures are triggered by the stimulus of bathing in hot water.
Although there is evidence of a genetic basis to its etiology, no gene associated with this disorder has so far been found.
In order to identify the genetic locus involved in the pathophysiology of hot water epilepsy, we performed a genome-wide linkage
analysis in a four-generation family manifesting the disorder in an autosomal dominant manner. Significant linkage was detected
on chromosome 4q24-q28, with the highest two-point LOD score of 3.50 at recombination value (θ) of 0 for the marker D4S402. Centromere-proximal and centromere-distal boundaries of this locus were defined by the markers
D4S1572 and D4S2277, respectively. The critical genetic interval spans 22.5 cM and corresponds to about 24 megabases of DNA.
The genes NEUROG2, ANK2, UGT8 and CAMK2D, which are known to be expressed in human brain, are strong positional candidates and we propose to examine these and other
genes in the locus to identify the causative gene for this intriguing form of epilepsy. 相似文献
17.
Hereditary lymphedema is a rare, lymphatic disorder resulting in the chronic swelling of the extremities. It shows wide inter-
and intra-familial clinical heterogeneity as well as variability in the age of onset. There are more than four genetically
distinct lymphedema conditions known and mutations in three genes have been discovered in families with lymphedema. However,
many other familial lymphedemas do not show linkage with the known loci, suggesting genetic heterogeneity. Here, we describe
a large inbred Pakistani family with congenital, progressive lymphedema confined to the lower limbs, which fades away at 40–45 years
of age. This condition segregates in an autosomal dominant fashion with reduced penetrance. The features are close to primary
lymphedema I, Nonne–Milory type (MIM 153100). We exclude this condition for linkage to the known loci for lymphedema by employing
highly polymorphic microsatellite markers from these intervals. Then, through a genome-wide linkage study we show that the
malformation in our family maps to chromosome 6q16.2–q22.1. The highest pair-wise LOD score (Z
max = 3.19) was obtained with microsatellite marker D6S1671, and a multipoint score of 3.75 was obtained at 108 cM. Haplotype
analysis indicated that the critical interval in this family flanks between markers D6S1716 and D6S303. Mutation analysis
in FOXO3, a likely candidate within this interval, did not show any pathogenic change in the affected family subjects. Our study provides
an evidence of a second locus for lymphedema type I. The discovery of the underlying gene could be helpful for the understanding
of this heterogeneous hereditary condition. 相似文献
18.
Postaxial Polydactyly (PAP) is characterized by fifth digit duplication in hands and/or feet. Two types of PAP including PAP-A,
representing the development of well-formed extra digit, and PAP-B, representing the presence of rudimentary fifth digit,
have been described. Both isolated and syndromic forms of PAP have been reported. Isolated forms of PAP usually segregate
as an autosomal dominant trait and to date four loci have been identified. In the present study, we have described mapping
of the first locus of autosomal recessive PAP type A on chromosome 13q13.3–13q21.2 in a consanguineous Pakistani family. Using
polymorphic microsatellite markers, the disease locus was mapped to a 17.87-cM (21.13 Mb) region flanked by markers D13S1288
and D13S632, on chromosome 13q13.3–13q21.2. A maximum multipoint LOD score of 3.84 was obtained with several markers along
the disease interval. DNA sequence analysis of exons and splice-junction sites of ten candidate genes (CHM-I, TSC22D1, FOXO1, DIAPH3, CCDC122, CKAP2, SUGT1, RANKL, LPAR6, C13ORF31) did not reveal potentially causal variants. 相似文献
19.
Multiple linkage regions have been reported in schizophrenia, and some appear to harbor susceptibility genes that are differentially expressed in postmortem brain tissue derived from unrelated individuals. We combined traditional genome-wide linkage analysis in a multiplex family with lymphocytic genome-wide expression analysis. A genome scan suggested linkage to a chromosome 4q marker (D4S1530, LOD 2.17, θ=0) using a dominant model. Haplotype analysis using flanking microsatellite markers delineated a 14 Mb region that cosegregated with all those affected. Subsequent genome-wide scan with SNP genotypes supported the evidence of linkage to 4q33–35.1 (LOD=2.39) using a dominant model. Genome-wide microarray analysis of five affected and five unaffected family members identified two differentially expressed genes within the haplotype AGA and GALNT7 (aspartylglucosaminidase and UDP-N-acetyl-alpha-D-galactosamine: polypeptide N-acetylgalactosaminyltransferase 7) with nominal significance; however, these genes did not remain significant following analysis of covariance. We carried out genome-wide linkage analyses between the quantitative expression phenotype and genetic markers. AGA expression levels showed suggestive linkage to multiple markers in the haplotype (maximum LOD=2.37) but to no other genomic region. GALNT7 expression levels showed linkage to regulatory loci at 4q28.1 (maximum LOD=3.15) and in the haplotype region at 4q33–35.1 (maximum LOD=2.37). ADH1B (alcohol dehydrogenase IB) was linked to loci at 4q21–q23 (maximum LOD=3.08) and haplotype region at 4q33–35.1 (maximum LOD=2.27). Seven differentially expressed genes were validated with RT-PCR. Three genes in the 4q33–35.1 haplotype region were also differentially expressed in schizophrenia in postmortem dorsolateral prefrontal cortex: AGA, HMGB2, and SCRG1. These results indicate that combining differential gene expression with linkage analysis may help in identifying candidate genes and potential regulatory sites. Moreover, they also replicate recent findings of complex trans- and cis- regulation of genes. 相似文献
20.
Caspase-2 is a member of the caspase family of cystein proteases involved in programmed cell death or apoptosis. Functional
and genetic data suggest it as a candidate gene for lymphopenia (Lyp)—a susceptibility gene for rat diabetes—which is responsible for the T-cell lymphopenia in the diabetes–prone BB rat. Firstly,
there is a higher frequency of apoptosis among recent thymic emigrants in the diabetes-prone BB rat than in the non-lymphopenic
diabetes-resistant BB rat. Secondly, caspase-2 maps close to Tcrb on mouse Chromosome (Chr) 6, while Lyp is closely linked to Tcrb on the homologous rat Chr 4. In this paper, we report genetic fine-positioning and radiation hybrid mapping of caspase-2
in the rat. Both methods positioned caspase-2 to rat Chr 4 between markers Prss1 and D4Mit5. Since Lyp maps distally to D4Mit5, between markers D4Rat75 and Npy, we exclude caspase-2 as a candidate gene for Lyp.
Received: 13 March 1998 / Accepted: 28 October 1998 相似文献