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Biomedical subjects

M Nissinen

Publications and source records attributed to M Nissinen.

At least 19 recordsLinked to original sources

Neurofibromatosis type 1 tumour suppressor gene expression is deficient in psoriatic skin in vivo and in vitro: a potential link to increased Ras activity.

BACKGROUND: Neurofibromatosis type 1 (NF1) protein (neurofibromin) accelerates the inactivation of Ras-GTP in various cell types. Somatic mutations of the NF1 gene may lead to malignant transformation and uncontrolled proliferation. We have previously shown that NF1 protein expression is downregulated in psoriasis in vivo. OBJECTIVES: To study the functional expression and distribution of NF1 mRNA and protein in vivo and in psoriatic and normal keratinocyte cultures. METHODS: Immunohistochemistry and in situ hybridization were used to study NF1 gene and protein expression in psoriasis in vivo. Furthermore, Northern and in situ hybridizations, immunoblot and localization analyses were utilized to study NF1 mRNA and protein in vitro in keratinocyte cultures. RESULTS: NF1 tumour suppressor gene expression was reduced in lesional psoriatic skin compared with perilesional and normal skin in vivo. The in vitro results showed that the levels of NF1 mRNA and protein were reduced in cultured psoriatic keratinocytes during cellular differentiation even after multiple passaging of the cells. Moreover, cultured nonlesional psoriatic keratinocytes were almost equally defective as lesional cells with respect to NF1 expression. CONCLUSIONS: Our findings demonstrate that psoriatic keratinocytes maintain an altered phenotype and gene expression profile even when isolated from interaction with lymphocytes and fibroblasts, which are known to increase proliferation of keratinocytes. As NF1 protein is regarded as a Ras proto-oncogene regulator, the aberrant expression and distribution of NF1 protein and mRNA found in the present study may be causative to the previously described increased activation of Ras in psoriatic lesions, and relate to altered cellular behaviour.

Blotting, Northern↗

Perceived stress, pain and work performance among non-patient working personnel with clinical signs of temporomandibular or neck pain.

The aim of the present study was to assess the associations between different types of perceived stress, pain and work performance among non-patients with clinical signs of muscle pain in the head/neck region. One-fifth (n = 241) of the 1339 media employees who had participated in a previous survey (Ahlberg J. et al., J Psychosom Res 2002; 53: 1077-1081) were randomly selected for standardized clinical examinations. Altogether 49% (n = 118) of these subjects had clinical signs of temporomandibular and/or neck muscle pain and were enrolled in the present study. The mean age of the study sample was 46.9 years (s.d. 6.6) and the female to male distribution 2:1. Of the 118 employees 46.5% reported that the pain problem interfered with their ability to work. Perceived ability to work was not significantly associated with age, gender or work positions. According to logistic regression, reduced work performance was significantly positively associated with continuous pain [odds ratio (OR) 4.38; 95% CI 1.21-15.7], level of perceived pain severity (OR 1.30; 95% CI 1.04-1.63), and health stress (OR 2.08; 95% CI 1.22-3.54). The results of this study indicated an association between specific self-reported stress regarding health and work issues, pain and work performance. From a preventive perspective this indicates a need for increased awareness about these associations on not only individual level but also at the organizational level and in health care.

Adult↗

Distinct biopsychosocial profiles emerge among nonpatients.

OBJECTIVES: The cross-sectional study comprised 30- to 55-year-old permanent employees (N=1784) of the Finnish Broadcasting Company (YLE). METHODS: The participants (N=1339, response rate 75%) completed standardised questionnaires covering demographic items, physical health, work performance, stress symptoms, pain and musculoskeletal symptoms, and overall biopsychosocial health. RESULTS: Physical symptoms (present often or continually) were reported by 15%, psychosomatic by 19% and psychosocial by 14%. The intercorrelations between 73 biopsychosocial variables revealed nine factors explaining 54.5% of variance for intrapersonal profiles and four factors explaining 59.2% of variance for interpersonal profiles. The Cronbach alphas for reliability ranged from.76 to.83. Three distinct biopsychosocial cluster profiles were found: Cluster 1 (n=290, 27%) loaded positively with the somatic and psychosocial variables, Cluster 2 (n=558, 51%) loaded negatively with the various biopsychosocial symptoms, and Cluster 3 (n=235, 22%) loaded positively with anxiety. CONCLUSION: Discriminant function analysis confirmed that this cluster solution correctly classified 95.2% of the subjects in a nonpatient multiprofessional population, which supports the biopsychosocial approach also in work life issues.

Adult↗

Reported bruxism and stress experience.

The aim of the study was to analyze whether perceived bruxism was associated with stress experience, age, gender, work role, and occupational health care use among a nonpatient multiprofessional population. Altogether, 1784 (age 30-55 years) employees of the Finnish Broadcasting Company were mailed a self-administered questionnaire covering demographics, perceived bruxism, total stress experience and the use of health care services provided by the company. The response rate was 75% (n = 1339, 51% men) and mean age was 46 years (SD = 6) in both genders. There were no significant differences in demographic status by age and gender. Bruxism and stress experiences did not significantly vary with regard to category of work, but both were significantly more frequent among women (P < 0.05). In all work categories frequent bruxers reported more stress, and the perceptions were significantly differently polarized between the groups (P < 0.001). According to logistic regression, frequent bruxism was significantly positively associated with severe stress experience (Odds ratio = 5.00; 95% CI = 2.84-8.82) and female gender (Odds ratio = 2.26; 95% CI = 1.43-3.55). Frequent bruxism was also significantly positively associated with the numbers of occupational health care and dental visits (P < 0.01), and slightly negatively associated with increasing age and work in administration (P < 0.05). It was concluded that bruxism may reveal ongoing stress in normal work life.

Administrative Personnel↗

Multiple sites of L-histidine decarboxylase expression in mouse suggest novel developmental functions for histamine.

Histamine mediates many types of physiologic signals in multicellular organisms. To clarify the developmental role of histamine, we have examined the developmental expression of L-histidine decarboxylase (HDC) mRNA and the production of histamine during mouse development. The predominant expression of HDC in mouse development was seen in mast cells. The HDC expression was evident from embryonal day 13 (Ed13) until birth, and the mast cells were seen in most peripheral tissues. Several novel sites with a prominent HDC mRNA expression were revealed. In the brain, the choroid plexus showed HDC expression at Ed14 and the raphe neurons at Ed15. Close to the parturition, at Ed19, the neurons in the tuberomammillary (TM) area and the ventricular neuroepithelia also displayed a clear HDC mRNA expression and histamine immunoreactivity (HA-ir). From Ed14 until birth, the olfactory and nasopharyngeal epithelia showed an intense HDC mRNA expression and HA-ir. In the olfactory epithelia, the olfactory receptor neurons (ORN) were shown to have very prominent histamine immunoreactivity. The bipolar nerve cells in the epithelium extended both to the epithelial surface and into the subepithelial layers to be collected into thick nerve bundles extending caudally toward the olfactory bulbs. Also, in the nasopharynx, an extensive subepithelial network of histamine-immunoreactive nerve fibers were seen. Furthermore, in the peripheral tissues, the degenerating mesonephros (Ed14) and the convoluted tubules in the developing kidneys (Ed15) showed HDC expression, as did the prostate gland (Ed15). In adult mouse brain, the HDC expression resembled the neuronal pattern observed in rat brain. The expression was restricted to the TM area in the ventral hypothalamus, with the main expression in the five TM subgroups called E1-E5. A distinct mouse HDC mRNA expression was also seen in the ependymal wall of the third ventricle, which has not been reported in the rat. The tissue- and cell-specific expression patterns of HDC and histamine presented in this work indicate that histamine could have cell guidance or regulatory roles in development.

Age Factors↗

A new potential toxaphene congener: synthesis, GC/EI-MS study, crystal structure, NMR analysis, and ab initio calculations of 3-endo,5-endo-dichloro-7,7-bis-chloromethyl-4-dichloromethyl-tricyclo[2.2.1.0(2,6)]heptane.

A new potential toxaphene congener 3-endo,5-endo-dichloro-7,7-bis-chloromethyl-4-dichloromethyl-tricyclo[2.2.1.0(2,6)]heptane 2 has been isolated from reaction mixture obtained by the chlorination of 2-exo, 10,10-trichlorobornane 1. The X-ray structural analysis of 2 revealed an unusual tricyclic structure, where the two chlorine atoms occupying endo-positions are in close spatial proximity with each other and near to the neighbouring CHCl2 group. Further, it revealed that the symmetry of the molecule is distorted. The 1H and 13C NMR spectra of 2 have been assigned by means of 1H, 1H double-quantum filtered correlation spectroscopy (DQF COSY), PFG 1H, 13C HMQC (pulsed field gradient heteronuclear multiple-quantum coherence), 1H, 13C heteronuclear multiple bond correlation (HMBC) experiments, and computer aided 1H NMR spectral analysis. The asymmetry of 2 is also discernible on the 1H NMR parameters. In addition, gas chromatographic (GC) properties and electron impact (EI) mass spectrum of 2 has been studied. Ab initio Hartree-Fock (HF) method with the basis set 6-31G(d) has been used for the optimization of the equilibrium geometry and calculation of total energy for 2. The optimized geometry is in good agreement with the crystal structure. According to the rotation energy profile calculated at the HF/6-31G(d) level, rotation of the chloromethyl and dichloromethyl groups are highly unlikely at the room temperature.

Environmental Pollutants↗

Selenium imides: 77Se NMR investigations of the SeCl2-tBuNH2 reaction and X-ray structures of Se3(NtBu)3, tBuNSe(mu-NtBu)2SO2, and tBuNSe(mu-NtBu)2SeO.

The reaction of SeCl2 with tert-butylamine in various molar ratios in THF at -78 degrees C has been investigated by 77Se NMR spectroscopy. In addition to the known Se-N heterocycles Se6(NtBu)2 (1) and Se9(NtBu)6 (2), the acyclic imidoselenium(II) dichlorides ClSe[N(tBu)Se]nCl (4, n = 1; 5, n = 2) and two new cyclic selenium imides [Se3(NtBu)2]n (3, n = 1 or 2) and Se3(NtBu)3 (6) have been isolated and identified. An X-ray analysis shows that 6 is a six-membered ring in a chair conformation with magnitude of d(Se-N) = 1.833 A. Crystal data: 6, trigonal, P3c1, a = 9.8660(3) A, c = 20.8427(7) A, V = 1757.0(1) A3, Z = 6. The 1H, 13C, and 77Se NMR data for 1-6 are reported, and some reassignments of earlier literature data for 1-3 (n = 1) are made. The decomposition of tBuN=Se=NtBu at 20 degrees C in toluene was monitored by 77Se NMR. The major products are 6 and 3. The Se(IV)-N systems tBuNSe(mu-NtBu)2E (7, E = SO2; 8, E = SeO) were prepared by the reaction of a mixture of SeCl4 and excess tBuNH2 with SO2Cl2 or SeOCl2, respectively. Compound 8 is also generated by the cycloaddition reaction of tBuNSeNtBu with tBuNSeO. Both 7 and 8 consist of slightly puckered four-membered rings. The mean terminal and bridging Se-N distances in 7 are 1.665(2) and 1.948(2) A, respectively. The corresponding values for 8 are 1.687(4) and 1.900(4) A, and d(Se=O) = 1.628(4) A. Crystal data: 7, monoclinic, P2(1)/c, a = 18.669(4) A, b = 12.329(2) A, c = 16.463(3) A, beta = 115.56(3) degrees, V = 3418.4(11) A3, Z = 4; 8, triclinic, P1, a = 6.372(1) A, b = 9.926(2) A, c = 14.034(3) A, alpha = 99.320(3) A, beta = 95.764(3) A, gamma = 103.876(3) A, V = 841.3(3) A3, Z = 2.

Journal Article↗

Psoriasis and altered calcium metabolism: downregulated capacitative calcium influx and defective calcium-mediated cell signaling in cultured psoriatic keratinocytes.

Intracellular calcium plays an important part in the regulation of proliferation and differentiation of keratinocytes. Detached from their in vivo environment, cultured psoriatic keratinocytes were investigated by monitoring free intracellular calcium concentration, which was measured using fura-2/AM as a calcium-sensitive probe. The mean increase in intracellular calcium of psoriatic keratinocytes was significantly reduced compared with control keratinocytes when intracellular calcium stores were mobilized from endoplasmic reticulum with thapsigargin. This finding suggests defective capacitative calcium influx of psoriatic cells. Intracellular calcium stores were similar in psoriatic and control keratinocytes, when extracellular calcium was chelated with ethyleneglycol-bis(beta-aminoethyl ether)-N,N,N',N',-tetraacetic acid and intracellular calcium was depleted with thapsigargin. Mechanical wounding of keratinocyte monolayer resulted in a significantly reduced rise in intracellular calcium of psoriatic cells in low (< 0.1 mM) and high (1.8 mM) extracellular calcium suggesting defective intercellular coupling of psoriatic keratinocytes. Blocking of gap-junctions with heptanol in wounded keratinocytes did not affect the intracellular calcium response in psoriatic keratinocytes in contrast to healthy keratinocytes. Adding adenosine triphosphate to culture medium resulted in a more pronounced intracellular calcium increase than thapsigargin in psoriatic keratinocytes, suggesting that inositol triphosphate-mediated, P2-purinergic signaling was enhanced in these cells. Moreover, psoriatic keratinocytes maintained their defective responses up to at least fifth passage suggesting that psoriatic keratinocytes have an inborn error in calcium metabolism, rather than a localized defect in response to altered extracellular calcium gradient observed in vivo.

Adenosine Triphosphate↗

Associations between thoracic kyphosis, head posture, and craniofacial morphology in young adults.

The aim of the present study was to investigate associations between thoracic hyper- and hypokyphosis, head posture, and craniofacial morphology in young adults. Using forward bending test and spinal pantographic measurements, 31 subjects, 16 with thoracic hyper- and 15 with hypokyphosis, were selected from a population-based cohort of 430 young adults. Lateral roentgen-cephalograms were taken in natural head posture and craniofacial and postural angular measurements were calculated. Any statistically significant differences between the groups thoracic hyperkyphosis and thoracic hypokyphosis--were analysed using Student's t test. Subjects with thoracic hyperkyphosis had a larger atlantocervical angle (At/ CVT, P < 0.01) than subjects with thoracic hypokyphosis. However, head position (NSL/VER) was similar in both groups, probably owing to the visual perception control of craniovertical relation. There was no statistically significant difference in craniofacial morphologyy between the groups.

Adult↗

Serum, biliary, and fecal cholesterol and plant sterols in colectomized patients before and during consumption of stanol ester margarine.

BACKGROUND: Cholesterol metabolic studies are simplified in colectomized patients because of rapid intestinal passage and reduced bacterial action. OBJECTIVE: Our objective was to study the effect on cholesterol and plant sterol metabolism of feeding a margarine containing stanol ester to 11 colectomized patients. DESIGN: A margarine containing 2 g stanol was consumed for 7-18 d. Serum, biliary, and fecal lipids were measured before and during consumption of the margarine. RESULTS: Serum cholesterol concentrations and the ratio of plant sterol to cholesterol decreased after 1 d of consumption of stanol esters (P < 0.05). After 7 d, serum cholesterol decreased by 16% (P < 0.01), cholesterol absorption efficiency decreased by approximately 40%, and fecal output of cholesterol as neutral sterols (but not as bile acids) increased by 36%. Biliary bile acid composition and the molar percentage of biliary cholesterol were unchanged. Increased ratios of cholesterol precursor sterols in serum and bile indicated enhanced cholesterol synthesis during consumption of stanol esters; the percentage absorption of plant sterols and the ratios of plant sterols to cholesterol decreased, whereas serum and biliary plant stanols and their biliary secretion gradually increased. In feces, 95% of cholesterol and 90% of plant stanols were in unesterified form. CONCLUSIONS: In colectomized patients, effective inhibition of cholesterol absorption and lowering of serum cholesterol concentrations and plant sterol ratios occurs within 1 d of the start of consumption of stanol esters. The composition of major bile lipids is unchanged, indicating that gallstone formation is unlikely. Small amounts of plant stanols are recovered in serum and bile during consumption of stanol esters but effectively are secreted through bile, thereby balancing the intake-induced increase in their absorption.

Adult↗

Positionally cloned gene for a novel glomerular protein--nephrin--is mutated in congenital nephrotic syndrome.

Congenital nephrotic syndrome of the Finnish type (NPHS1) is an autosomal-recessive disorder, characterized by massive proteinuria in utero and nephrosis at birth. In this study, the 150 kb critical region of NPHS1 was sequenced, revealing the presence of at least 11 genes, the structures of 5 of which were determined. Four different mutations segregating with the disease were found in one of the genes in NPHS1 patients. The NPHS1 gene product, termed nephrin, is a 1241-residue putative transmembrane protein of the immunoglobulin family of cell adhesion molecules, which by Northern and in situ hybridization was shown to be specifically expressed in renal glomeruli. The results demonstrate a crucial role for this protein in the development or function of the kidney filtration barrier.

Amino Acid Sequence↗

Genetics of laminin alpha 2 chain (or merosin) deficient congenital muscular dystrophy: from identification of mutations to prenatal diagnosis.

Congenital muscular dystrophies (CMD) are a clinically and genetically heterogeneous group of muscle disorders, with autosomal recessive inheritance. Absence of the laminin alpha 2 chain in the skeletal muscle of patients with classical CMD has permitted the identification of a subgroup, referred to as 'merosin-deficient CMD or laminin alpha 2 chain deficient CMD'. We first identified a nonsense and a splice site mutation in laminin alpha 2 gene (LAMA2) (Glu1241 stop, 4573-2A-->T). We report here new mutations: nonsense mutations (Glu210stop, Trp2316stop) and 1- and 2-bp deletions (2418 delta C, 6968 delta TA), which result in truncation of the protein either in the short arm domains or in the C terminal globular domain and complete merosin deficiency. Another subgroup, referred to as 'partially-deficient in laminin alpha 2 chain' has been identified recently, and a LAMA2 missense mutation (Cys996Arg) has been shown to cause this partial deficiency. The laminin alpha 2 chain, together with the beta 1 or beta 2 and gamma 1 chains forms either laminin-2 (alpha 2-beta 1-gamma 1) or laminin-4 (alpha 2-beta 2-gamma 1). The LAMA2 mutations induce the formation of abnormal laminins which probably dramatically disturb the assembly and stability of the laminin network, one of the major components of the extracellular matrix in skeletal muscle. We report also the first prenatal diagnosis performed by direct mutation analysis.

Chromosome Mapping↗

Substitution of a conserved cysteine-996 in a cysteine-rich motif of the laminin alpha2-chain in congenital muscular dystrophy with partial deficiency of the protein.

Congenital muscular dystrophies (CMDs) are autosomal recessive muscle disorders of early onset. Approximately half of CMD patients present laminin alpha2-chain (merosin) deficiency in muscle biopsies, and the disease locus has been mapped to the region of the LAMA2 gene (6q22-23) in several families. Recently, two nonsense mutations in the laminin alpha2-chain gene were identified in CMD patients exhibiting complete deficiency of the laminin alpha2-chain in muscle biopsies. However, a subset of CMD patients with linkage to LAMA2 show only partial absence of the laminin alpha2-chain around muscle fibers, by immunocytochemical analysis. In the present study we have identified a homozygous missense mutation in the alpha2-chain gene of a consanguineous Turkish family with partial laminin alpha2-chain deficiency. The T-->C transition at position 3035 in the cDNA sequence results in a Cys996-->Arg substitution. The mutation that affects one of the conserved cysteine-rich repeats in the short arm of the laminin alpha2-chain should result in normal synthesis of the chain and in formation and secretion of a heterotrimeric laminin molecule. Muscular dysfunction is possibly caused either by abnormal disulfide cross-links and folding of the laminin repeat, leading to the disturbance of an as yet unknown binding function of the laminin alpha2-chain and to shorter half-life of the muscle-specific laminin-2 and laminin-4 isoforms, or by increased proteolytic sensitivity, leading to truncation of the short arm.

Amino Acid Sequence↗

Left handedness and risk of thoracic hyperkyphosis in prepubertal schoolchildren.

BACKGROUND: Hand dominance and spinal posture were studied for their prediction of the development of thoracic hyperkyphosis during the pubertal growth spurt. METHODS: The cohort consisted of all the fourth-grade school children of the Western School District of Helsinki, Finland, in the spring of 1986. They were examined annually from the mean age of 10.8 to 13.8 years. Handedness was determined at the baseline examination by observing the hand with which the child was writing. Anthropometric measurements, posture and growth were followed-up annually. A lateral standing radiograph was undertaken in those children who had pronounced thoracic kyphosis in spinal pantography. Kyphotic angles > or = 45 degrees were considered hyperkyphotic. RESULTS: In both girls and boys, left handedness was found to be a powerful determinant of hyperkyphosis. In left handed children the odds ratio (OR), adjusted for baseline spinal measurements, was 4.11 (95% confidence interval [CI]: 1.39-12.13). Hump size measured by the forward bending test also predicted significantly the development of thoracic hyperkyphosis (OR = 1.48; 95% CI: 1.23-1.76, per one degree). CONCLUSIONS: Left handedness may be a risk factor for thoracic hyperkyphosis during the pubertal growth spurt.

Anthropometry↗

Spinal posture during pubertal growth.

A cohort of children was followed-up annually from a mean age of 10.8-13.8 years to determine the development of their posture. Of the sample of 1060 children, 847 (79.9%) participated in the final examination. Thoracic kyphosis and lumbar lordosis were measured annually with a spinal pantograph. Those children whose thoracic kyphosis in pantography was more than 35 degrees at entry and 45 degrees or more at the final examination underwent a lateral standing radiograph. The 3-year incidence of Scheurermann's disease was 0.4%. The mean thoracic kyphosis increased and the mean lumbar lordosis decreased with age in both sexes, but these changes were not constant. Thoracic kyphosis was most pronounced at a mean age of 12.8 years and lumbar lordosis was least pronounced at a mean age of 13.8 years. In accordance with the literature, the wide individual variation found in this study for both thoracic kyphosis and lumbar lordosis during the pubertal growth period was mainly physiologic.

Adolescent↗

Anthropometric measurements and the incidence of low back pain in a cohort of pubertal children.

STUDY DESIGN: The authors studied the anthropometric measurements to predict low back pain (LBP) in a cohort of growing adolescents. SUMMARY OF BACKGROUND DATA: The cohort consisted of all the fourth-grade school children of the western school district of Helsinki, Finland, in the spring of 1986. They were examined annually from the mean age of 11.8 to 13.8 years. METHODS: The forward bending test, measurements of total arm length, pelvic equilibrium, and spinal pantographs were carried out by the same physiatrist. A standardized pain questionnaire presented at the final examination obtained the history of LBP. Of the original cohort of 1060 children, those 859 (408 girls and 451 boys) who participated in all the examinations and had not had LBP until the age of 12.8 years were included in this study. RESULTS: The 1-year (from 12.8 to 13.8 years) incidence of LBP was 18.4% in girls and 16.9% in boys. Trunk asymmetry measured by the forward bending test and sitting height were significant determinants of the incidence of LBP. In the whole cohort, the odds ratio (OR) of trunk asymmetry adjusted for all the other risk determinants was 1.19 and its confidence interval (CI) was 1.00-1.39 per one standard deviation increase of the trunk hump. In the multivariate analysis comprising both sexes, OR per one standard deviation increase of sitting height was 1.24, (95% CI 1.03-1.46). In boys, standing height (OR 1.40, 95% CI 1.13-1.65, per one standard deviation) and sitting height (OR 1.35, 95% CI 1.09-1.63, per one standard deviation) were positively associated with the risk of LBP. These associations were not significant in girls. CONCLUSIONS: Sitting height and trunk asymmetry may contribute to LBP in pubertal children. The role of anthropometric characteristics seems, however, modest.

Adolescent↗

Human laminin M chain (merosin): complete primary structure, chromosomal assignment, and expression of the M and A chain in human fetal tissues.

The primary structure of the human laminin M chain was determined from cDNA clones isolated from human placental libraries. The clones covered a total of 6,942 bp, with 49-bp encoding a 5' end untranslated region and 6,893-bp coding for a translated sequence. The complete human laminin M chain contains a 22-residue signal peptide and 3,088 residues of the mature M chain. The M chain has a domain structure similar to that of the human and mouse A chains. The homology between the two human laminin heavy chains is highest in the short arm region and lowest in the long arm helical domain I + II. Northern blot analysis of human fetal tissues showed that the M chain was expressed in most tissues such as cardiac muscle, pancreas, lung, spleen, kidney, adrenal gland, skin, testis, meninges, choroid plexus, and some other regions of the brain, but not in liver, thymus, and bone. In situ hybridization localized the expression of the M chain gene to cells of mesenchymal origin. In contrast, expression of the A chain was observed only in kidney, testis, neuroretina and some region of brain as determined by Northern analyses. Epithelial and endothelial cells were negative for both M and A chain gene transcripts. The gene for the human M chain (LAMM) was localized to chromosome 6q22-->23.

Amino Acid Sequence↗