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Biomedical subjects

Lei Zhang

Publications and source records attributed to Lei Zhang.

At least 361 records · Page 20Linked to original sources
PubMed2003

Cyclin-dependent kinase-5 is involved in neuregulin-dependent activation of phosphatidylinositol 3-kinase and Akt activity mediating neuronal survival.

The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway plays an important role in mediating survival signals in wide variety of neurons and cells. Recent studies show that Akt also regulates metabolic pathways to regulate cell survival. In this study, we reported that cyclin-dependent kinase-5 (Cdk5) regulates Akt activity and cell survival through the neuregulin-mediated PI 3-kinase signaling pathway. We found that brain extracts of Cdk5-/-mice display a lower PI 3-kinase activity and phosphorylation of Akt compared with that in wild type mice. Moreover, we demonstrated that Cdk5 phosphorylated Ser-1176 in the neuregulin receptor ErbB2 and phosphorylated Thr-871 and Ser-1120 in the ErbB3 receptor. We identified the Ser-1120 sequence RSRSPR in ErbB3 as a novel phosphorylation consensus sequence of Cdk5. Finally, we found that Cdk5 activity is involved in neuregulin-induced Akt activity and neuregulin-mediated neuronal survival. These findings suggest that Cdk5 may exert a key role in promoting neuronal survival by regulating Akt activity through the neuregulin/PI 3-kinase signaling pathway.

Amino Acid Sequence↗
PubMed2003

Cloning, expression, and characterization of a human 4'-phosphopantetheinyl transferase with broad substrate specificity.

A single candidate 4'-phosphopantetheine transferase, identified by BLAST searches of the human genome sequence data base, has been cloned, expressed, and characterized. The human enzyme, which is expressed mainly in the cytosolic compartment in a wide range of tissues, is a 329-residue, monomeric protein. The enzyme is capable of transferring the 4'-phosphopantetheine moiety of coenzyme A to a conserved serine residue in both the acyl carrier protein domain of the human cytosolic multifunctional fatty acid synthase and the acyl carrier protein associated independently with human mitochondria. The human 4'-phosphopantetheine transferase is also capable of phosphopantetheinylation of peptidyl carrier and acyl carrier proteins from prokaryotes. The same human protein also has recently been implicated in phosphopantetheinylation of the alpha-aminoadipate semialdehyde dehydrogenase involved in lysine catabolism (Praphanphoj, V., Sacksteder, K. A., Gould, S. J., Thomas, G. H., and Geraghty, M. T. (2001) Mol. Genet. Metab. 72, 336-342). Thus, in contrast to yeast, which utilizes separate 4'-phosphopantetheine transferases to service each of three different carrier protein substrates, humans appear to utilize a single, broad specificity enzyme for all posttranslational 4'-phosphopantetheinylation reactions.

Amino Acid Sequence↗
PubMed2003

Surface-exposed tryptophan residues are essential for O-acetylserine sulfhydrylase structure, function, and stability.

O-Acetylserine sulfhydrylase is a homodimeric enzyme catalyzing the last step of cysteine biosynthesis via a Bi Bi ping-pong mechanism. The subunit is composed of two domains, each containing one tryptophan residue, Trp50 in the N-terminal domain and Trp161 in the C-terminal domain. Only Trp161 is highly conserved in eucaryotes and bacteria. The coenzyme pyridoxal 5'-phosphate is bound in a cleft between the two domains. The enzyme undergoes an open to closed conformational transition upon substrate binding. The effect of single Trp to Tyr mutations on O-acetylserine sulfhydrylase structure, function, and stability was investigated with a variety of spectroscopic techniques. The mutations do not significantly alter the enzyme secondary structure but affect the catalysis, with a predominant influence on the second half reaction. The W50Y mutation strongly affects the unfolding pathway due to the destabilization of the intersubunit interface. The W161Y mutation, occurring in the C-terminal domain, produces a reduction of the accessibility of the active site to acrylamide and stabilizes thermodynamically the N-terminal domain, a result consistent with stronger interdomain interactions.

Acrylamide↗
PubMed2003

TNF-alpha acutely inhibits vascular effects of physiological but not high insulin or contraction.

TNF-alpha is elevated in many states of insulin resistance, and acutely administered TNF-alpha in vivo inhibits insulin-mediated hemodynamic effects and glucose uptake in muscle. In this study, we assess whether the inhibitory effects of TNF-alpha are affected by insulin dose or muscle contraction. Whole body glucose infusion rate (GIR), femoral blood flow (FBF), hindleg vascular resistance, hindleg glucose uptake (HGU), 2-deoxyglucose uptake into muscles of the lower leg (R'g) and hindleg metabolism of infused 1-methylxanthine (1-MX), a measure of capillary recruitment, were determined. Three groups were studied with and without infusion of TNF-alpha: euglycemic insulin-clamped, one-leg field-stimulated (2 Hz, 0.1 ms at 30 V), and saline-infused control anesthetized rats. Insulin infusions were 3, 10, or 30 mU x kg-1 x min-1 for 2 h x 1-MX metabolism was maximally increased by all three doses of insulin. GIR, HGU, and R'g were maximal at 10 mU and FBF was maximal at 30 mU of insulin. Contraction increased FBF, HGU, and 1-MX. TNF-alpha (0.5 microg x kg-1 x h-1) totally blocked the 3 and 10 mU insulin-mediated increases in FBF and 1-MX, and partly blocked GIR, HGU, and R'g. None of the increases due to twitch contraction was affected by TNF-alpha, and only the increase in FBF due to 30 mU of insulin was partly affected. We conclude that muscle capillary recruitment and glucose uptake due to high levels of insulin or muscle contraction under twitch stimuli at 2 Hz are resistant to TNF-alpha. These findings may have implications for ameliorating muscle insulin resistance resulting from increased plasma TNF-alpha and for the differing mechanisms by which contraction and insulin recruit capillary flow in muscle.

Animals↗
PubMed2003

Role of cysteine S-conjugate beta-lyase in the metabolism of cisplatin.

Cisplatin is nephrotoxic, but the mechanism by which cisplatin kills renal proximal tubule cells is not well defined. Inhibition of gamma-glutamyl transpeptidase or pyridoxal 5'-phosphate (PLP)-dependent enzymes blocks the nephrotoxicity. Our hypothesis is that cisplatin is metabolized to a renal toxin through a platinum-glutathione conjugate to a reactive sulfur-containing compound. The final step in this bioactivation is the conversion of a platinum-cysteine S-conjugate to a reactive thiol by a PLP-dependent cysteine S-conjugate beta-lyase. LLC-PK1 cells, a proximal tubule cell line with low cysteine S-conjugate beta-lyase activity, are used to study cisplatin nephrotoxicity. We proposed that the beta-elimination reaction catalyzed by cysteine S-conjugate beta-lyase is the rate-limiting step in the metabolism of cisplatin to a toxin in these cells. In this study, LLC-PK1 cells were transfected with human glutamine transaminase K, which catalyzes the beta-elimination reaction. Cisplatin was significantly more toxic in confluent monolayers of cells with increased cysteine S-conjugate beta-lyase activity. In contrast, carboplatin, a non-nephrotoxic derivative of cisplatin, was 20-fold less toxic than cisplatin in confluent cells, and its toxicity was not altered by overexpression of cysteine S-conjugate beta-lyase. We propose that carboplatin is not nephrotoxic because it is not metabolized through this pathway. Dividing cells were more sensitive to both cisplatin and carboplatin toxicity. Overexpression of cysteine S-conjugate beta-lyase activity had no effect on the toxicity of either drug. These data demonstrate that cisplatin kills quiescent renal cells by a mechanism that is distinct from the mechanism by which it kills dividing cells and that the renal toxicity of cisplatin is dependent on cysteine S-conjugate beta-lyase activity.

Animals↗
PubMed2003

Inactivation of DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation and its relation to p53 mutations in esophageal squamous cell carcinoma.

The development of esophageal squamous cell carcinoma (ESCC) has been linked to exposure to carcinogens such as nitrosamines that cause various alkyl DNA damages and O6-methylguanine-DNA methyltransferase (MGMT) is a primary defence against alkylation-induced mutagenesis and carcinogenesis. This study was to investigate the role of inactivation of MGMT by promoter hypermethylation and its relation to p53 mutations in ESCC. Methylation of MGMT promoter was determined by methylation-specific polymerase chain reaction in 119 ESCC specimens, 22 corresponding tissue samples adjacent to the tumors, and 21 normal epithelial specimens of the esophagus. The levels of MGMT protein in ESCC with methylated or unmethylated MGMT were analyzed by quantitative immunohistochemistry. Mutations of p53 in 119 ESCC were detected by denaturing high-performance liquid chromatography and sequencing. We found that all 21 normal esophageal tissues had unmethylated MGMT; however, among 119 ESCC, 46 (38.7%) had hypermethylated MGMT. This epigenetic change also occurred in some normal tissues adjacent to the tumors. The level of MGMT protein in MGMT-methylated ESCC was significantly lower than that in MGMT-unmethylated ESCC, whereas great inter-individual variation and poor expression was also observed among MGMT-unmethylated ESCC. Fifty-one percent (61/119) ESCC showed p53 mutations but the distribution of the mutations did not differ significantly between MGMT-methylated ESCC (44%) and MGMT-unmethylated ESCC (56.2%; P = 0.18). MGMT promoter hypermethylation was neither associated with overall G:C to A:T mutations nor associated with this type of mutations in non-CpG dinucleotides in p53. Our results demonstrate that inactivation of MGMT by aberrant promoter methylation is a frequent molecular event in ESCC. This epigenetic alteration is an important, but may not be the sole, mechanism leading to the impaired expression of MGMT. Aberrant MGMT methylation seemed not to be associated with overall frequency and spectrum of p53 mutations in ESCC.

Carcinoma, Squamous Cell↗
PubMed2003

A ferromagnetically coupled CrCu3 tetramer and GdCu4 pentamer with a [15]N4 macrocylic ligand incorporating an oxamido bridge.

The synthesis and structural and magnetic properties of heteropolynuclear complexes [(L(3)Cu)(3)Cr](CH(3)CN)(3)(ClO(4))(3) (2) and [(L(3)Cu)(4)Gd.H(2)O](CH(3)OH)(H(2)O)(ClO(4))(3) (3) (H(2)L(3) ligand is 2,3-dioxo-5,6:14,15-dibenzo-1,4,8,12-tetraazacyclo-pentadeca-7,12-diene) and their precursor L(3)Cu (1) are presented. Complex 2 crystallizes in space group P2(1)/n with cell parameters a = 20.828(6) A, b = 18.321(5) A, c = 7.578(5) A, alpha = 90 degrees, beta = 91.990(8) degrees, gamma = 90 degrees, and Z = 4. The Cr(III) center is coordinated by six oxygen atoms from three Cu(II) precursors. The Cr-O bonds range over 1.948-1.982 A. The coordination environments of all the terminal Cu(II) ions change in comparison with their Cu(II) precursor. The ferromagnetic coupling (J = 16.48(1) cm(-)(1)) observed for 2 can be rationalized by symmetry considerations. For any pair of interacting magnetic orbitals, strict orthogonality is obeyed and the interaction is ferromagnetic. Complex 3 crystallizes in space group P1 with cell parameters a = 14.805(4) A, b = 16.882(5) A, c = 17.877(5) A, alpha = 75.403(5) degrees, beta = 83.317(6) degrees, gamma = 70.600(5) degrees, and Z = 2. The central Gd(III) assumes an 8 + 1 coordination environment, namely eight oxygen atoms from four Cu(II) precursors and one oxygen atom from H(2)O. The fit of the experimental data gives J = 0.27(2) cm(-)(1), g(Gd) = 1.98(1), and g(Cu) = 2.05(1). This small and positive J value shows weak ferromagnetic interaction between metal ions.

Journal Article↗
PubMed2003

Protein-protein interaction map for yeast TFIID.

A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID. TFIID is composed of TATA binding protein (TBP) and approximately a dozen TBP-associated factors (TAFs). Emerging consensus regarding the role of TAFs is that TFIID assumes a gene specific activity that is regulated by interaction with other factors. In spite of many studies demonstrating the essential nature of TAFs in transcription, very little is known about the subunit contacts within TFIID. To understand fully the functional role of TAFs, it is imperative to define TAF-TAF interactions and their topological arrangement within TFIID. We performed a systematic two-hybrid analysis using the 13 essential TAFs of the Saccharomyces cerevisiae TFIID complex and TBP. Specific interactions were defined for each component, and the biological significance of these interactions is supported by numerous genetic and biochemical studies. By combining the interaction profiles presented here, and the available studies utilizing specific TAFs, we propose a working hypothesis for the arrangement of components in the TFIID complex. Thus, these results serve as a foundation for understanding the overall architecture of yeast TFIID.

Protein Binding↗
PubMed2003

Sex-related differences in neuronal cell survival and signaling in rats.

While substantial and compelling evidence exists for sex-related differences in gross and microscopic brain structure, our understanding of the cellular mechanisms that give rise to these sexual dimorphisms is in its infancy. To investigate possible underlying mechanisms for sex-related differences in neuronal development, we examined neuronal survival and transductional signaling in male and female rat primary cortical neuronal cultures. We found that following 14 days in culture, the total number of surviving neurons was significantly higher in female cultures derived from either cortical plate (cp) or ventricular zone (vz), the regions where differentiating (cp) and proliferating (vz) cells are located. In addition, sex-related differences in the levels of phospho-ERK1 and Akt were also observed. Female cortical cultures had significantly higher levels of ERK1 in both cp and vz and higher levels of Akt in cp. No sex-related differences in Bcl-2 were observed. These data suggest that dimorphisms in cell survival may underlie enhanced neuronal survival (or decreased apoptosis) in female brain. Further, the appearance of sex-related differences at cellular and signaling levels in cortical neuronal cultures demonstrates that the effects of gender are not limited to parts of the brain mediating reproduction.

Animals↗
PubMed2003

Gas chromatographic method for detection of urinary sucralose: application to the assessment of intestinal permeability.

We developed a capillary column gas chromatography (CCGC) method for the measurement of urinary sucralose (S) and three other sugar probes including, sucrose, lactulose (L) and mannitol (M) for use in in vivo studies of intestinal permeability. We compared the capillary method with a packed column gas chromatography (PCGC) method. We also investigated a possible role for sucralose as a probe for the measurement of whole gut permeability. Sample preparation was rapid and simple. The above four sugars were detected precisely, without interference. We measured intestinal permeability using 5- and 24-h urine collections in 14 healthy volunteers. The metabolism of sugars was evaluated by incubating the intestinal bacteria with an iso-osmolar mixture of mannitol, lactulose and sucralose at 37 degrees C for 19 h. Sugar concentrations and the pH of the mixture were monitored. The use of the CCGC method improved the detection of sucralose as compared to PCGC. The average coefficient of variation decreased from 15% to 4%. It also increased the sensitivity of detection by 200-2000-fold. The GC assay was linear between sucralose concentrations of 0.2 and 40 g/l (r=1.000). Intestinal bacteria metabolized lactulose and acidified the media but did not metabolize sucralose or mannitol. The new method for the measurement of urinary sucralose permits the simultaneous quantitation of sucrose, mannitol and lactulose, and is rapid, simple, sensitive, accurate and reproducible. Because neither S nor M is metabolized by intestinal bacteria, and because only a tiny fraction of either sugar is absorbed, this pair of sugar probes appears to be available for absorption throughout the GI tract. Thus, the 24-h urinary concentrations of S and M, or the urinary S/M ratio following an oral dose of a sugar mixture, might be good markers for whole gut permeability.

Chromatography, Gas↗
PubMed2003

Neural basis of the non-attentional processing of briefly presented words.

The neural basis of the automatic activation of words was investigated in an fMRI study. In the study, words were presented briefly (51 or 151 msec) followed by a mask. To prevent attentional processing, subjects attended to the masks and not the words, and were required to make perceptual judgment about the masks. We found that a distributed neural network (including the frontal, temporal, occipital, parietal lobes, and the cerebellum) was activated during non-attentional processing of words in both exposure durations. A significant main effect of presentation duration was found in bilateral cerebellum and the right fusiform gyrus, suggesting their role in the later (151 msec) processing of words. In addition, a significant interaction between presentation duration and word frequency was obtained. When the presentation duration was 151 msec, no significant difference in activation was found between high- and low-frequency words. Alternatively, when the presentation duration was 51 msec, high-frequency words evoked significantly greater activation in bilateral fusiform gyri, cerebellum, right inferior parietal lobe, medial frontal gyrus (BA 45/46/9), and the right temporal-occipital junction (BA 21/37). These results suggest that these regions are sensitive to word frequency, and are related to both the attentional and non-attentional access of lexical representations.

Adolescent↗
PubMed2003

Axonal regeneration of descending and ascending spinal projection neurons in spinal cord-transected larval lamprey.

The distributions of descending and ascending spinal projection neurons (i.e., spinal neurons with moderate to long axons) were compared in normal larval lamprey and in animals that had recovered for 8 weeks following a complete spinal cord transection at 50% body length (BL, normalized distance from the anterior head). In normal animals, application of HRP to the spinal cord at 60% BL (40% BL) labeled an average of 713.8 +/- 143.2 descending spinal projection neurons (718.4 +/- 108.0 ascending spinal projection neurons) along the rostral (caudal) spinal cord, most of which were unidentified neurons. Some of these neurons project for at least approximately 50-60 spinal cord segments (approximately 36-47 mm in animals with an average length of approximately 90 mm used in the present study). At 8 weeks posttransection, the numbers of HRP-labeled descending or ascending spinal neurons that extended their axons through the transection were about 40% of those in similar areas of the spinal cord in normal animals. Thus, in larval lamprey, axonal regeneration of descending and ascending spinal projection neurons is incomplete, similar to that found for descending brain neurons. The majority of restored projections were from unidentified spinal neurons that have not been documented previously. In contrast to results from several other lower vertebrates, in the lamprey ascending spinal neurons exhibited substantial axonal regeneration. Identified descending spinal neurons, such as lateral interneurons and crossed contralateral interneurons, and identified ascending spinal neurons, such as giant interneurons and edge cells, regenerated their axons at least 9 mm beyond the transection site in animals with an average length of approximately 90 mm, which is appreciably farther than previously reported. In contrast, most dorsal cells, which are centrally located sensory neurons, exhibited very little axonal regeneration.

Animals↗
PubMed2003

Congenital diaphragmatic hernia, kidney agenesis and cardiac defects associated with Slit3-deficiency in mice.

Slit3 along with Slit1 and Slit2 comprise the Slit family of proteins. The latter two proteins are known to be involved in axon guidance and cell migration during animal development. However, little is know about the functions of Slit3. We created a Slit3-deficient mouse model from an OmniBank ES cell line with a Slit3 allele trapped by insertional mutagenesis to analyze the in vivo functions of this protein. In this model, congenital diaphragmatic hernia is the most obvious phenotype. Herniation was found to be caused by a defective central tendon (CT) of the diaphragm that remained fused with the liver. Electron microscopic analyses of the defective CT revealed disorganized collagen fibrils that failed to form tight collagen bundles. The hearts of Slit3-deficient mice have an enlarged right ventricle. In addition, 20% of homozygous mice also showed a range of kidney defects that include unilateral or bilateral agenesis of the kidney and ureter, or varying degrees of renal hypoplasia. Thus, we concluded that Slit3 is involved in the development of multiple organ systems that include the diaphragm and the kidney. Slit3-deficient mice represent a genetic animal model for physiological and pathological studies of congenital diaphragmatic hernia.

Animals↗
PubMed2003

Calmodulin-binding protein kinases in plants.

Many calmodulin-binding protein kinases have been isolated from plants. Plant calmodulin-binding protein kinases are novel protein kinases that differ from calcium-dependent protein kinases in many important respects. Calmodulin-binding protein kinases are likely to be crucial mediators of responses to diverse endogenous and environmental cues in plants. In this update, we review the structure, regulation, expression and possible functions of plant calmodulin-binding protein kinases.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed2003

Expression of Drosophila Ca2+ permeable transient receptor potential-like channel protein in a prostate cancer cell line decreases cell survival.

The effects of expression of Drosophila melanoga ster Ca(2+) permeable transient receptor potential-like (TRPL) channels, under the control of the cytomegalovirus (CMV) or prostate cell-specific promoters, on cell survival and apoptosis in the androgen-sensitive LNCaP prostate cancer cell line were investigated. A prostate-specific antigen (PSA) promoter construct (designated PSAEn/PSAPr) composed of a 0.6 kb region of the promoter and a 1.45 kb region of the enhancer resulted in androgen-dependent and prostate-specific expression of a luciferase reporter gene in transiently transfected LNCaP cells. Expression of the enhanced green fluorescence protein-TRPL chimeric protein under the control of the CMV promoter was confirmed by Western blot. Whereas the majority of the expressed protein was located in the cytoplasmic space, confocal microscopy with the CD-9 protein as a plasma membrane marker demonstrated that approximately 10% of the expressed TRPL protein was located in a band in the plasma membrane. Using recombinant adenoviruses, expression of the TRPL protein was associated with an increase in both the initial and sustained rates of Ca(2+) inflow. Expression of TRPL under the control of the CMV promoter for 96 hours decreased cell number and increased the number of cells undergoing apoptosis by 23 and 27%, respectively. Apoptosis was inhibited by a caspase-3 inhibitor, Z-DEVD-fmk. It is concluded that, when heterologously expressed in LNCaP cells, the TRPL protein leads to a reduction in cell survival due, in part, to the induction of apoptosis. The effects of TRPL are likely caused by enhanced Na(+) and Ca(2+) inflow to the cells. This finding suggests a novel approach to modify the growth of prostate cancer cells that fail to undergo apoptosis following androgen ablation therapy.

Adenoviridae↗
PubMed2003

Epidemiology of spine tumors presenting to musculoskeletal physiatrists.

OBJECTIVE: To report the incidence and epidemiologic formation of previously undetected primary and secondary spine tumors presenting as spinal and/or extremity pain to a physiatrist practicing in an academic or private practice multidisciplinary spine center. DESIGN: Multicenter retrospective chart review. SETTING: Three multidisciplinary spine settings (1 academic, 2 private). PARTICIPANTS: Charts of patients from 33 academic and 18 private practice settings. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Epidemiologic data collected included incidence, age, gender, race, and duration of symptoms before initial presentation. Symptom presentation data collected included intensity of pain when supine, sitting, standing, or walking; character of the pain; pain intensity as measured on the visual analog scale (VAS); spontaneous versus traumatic etiology; unexplained weight loss; presence of night pain; and fever. In addition, the results of radiographic studies including plain films, imaging, bone scan, and magnetic resonance imaging were recorded. The type of neoplastic disease was also assessed, primary versus metastatic, as well as the metastatic source. RESULTS: The incidence of spine tumors was.69% in academic multidisciplinary spine centers and.12% in private practice multidisciplinary spine centers. Patients with spinal pain because of neoplastic disease who presented to musculoskeletal physiatrists were an average age of 65.3 years and reported a relatively high likelihood of night pain, aching character of symptom manifestation, spontaneous onset of symptoms, history of cancer, standing and walking provoking symptoms, and unexplained weight loss. In addition, the pain intensity level ranged widely, with an average VAS score of 6.8. CONCLUSIONS: There are many similarities and differences in the clinical presentation of patients with spinal pain from spine tumors who present to musculoskeletal physiatrists practicing in multidisciplinary spine centers when compared with those presenting to a primary care setting.

Adult↗
PubMed2003

Molecular cloning and characterization of a mannose-binding lectin gene from Crinum asiaticum.

Full-length cDNA of a mannose-binding lectin or agglutinin gene was cloned from a traditional Chinese medicinal herb Crinum asiaticum var. sinicum through RACE-PCR cloning. The full-length cDNA of C. asiaticum agglutinin (caa) was 820 bp and contained a 528 bp open reading frame encoding a lectin precursor (preproprotein) of 175 amino acid residues with a 22 aa signal peptide. The coding region of the caa gene was high in G/C content. The first 20 bp of the 5' UTR had a dC content of 50%, which was a typical feature of the leader sequence. By cutting away the signal peptide, the CAA proprotein was 15.79 kDa with a pl of 9.27 and contained 3 mannose-binding sites (QDNY). Random coil and extended strand constituted interlaced domination of the main part of the secondary structure. B-lectin conserved domain existed within N24 to G130. Predicted three-dimensional structure of CAA proprotein was very similar to that of GNA (Galanthus nivalis agglutinin). It is significant that besides certain homologies to known monocot mannose-binding lectins from Amaryllidaceae, Orchidaceae, Alliaceae and Liliaceae, caa also showed high similarity to gastrodianin type antifungal proteins. No intron was detected within the region of genomic sequence corresponding to the caa full-length cDNA. Southern blot analysis indicated that the caa gene belonged to a low-copy gene family. Northern blot analysis demonstrated that caa mRNA was constitutively expressed in all the tested tissue types including the root, bulb, leaf, rachise, flower and fruit tissues.

Amino Acid Sequence↗