Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “colocalization analysis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,531 records · Page 85Linked to original sources
PubMed2004

Endothelial lipase is synthesized by hepatic and aorta endothelial cells and its expression is altered in apoE-deficient mice.

Both LPL and HL are synthesized in parenchymal cells, are secreted, and bind to endothelial cells. To learn where endothelial lipase (EL) is synthesized in adult animals, the localization of EL in mouse and rat liver was studied by immunohistochemical analysis. Furthermore, to test whether EL could play a role in atherogenesis, the expression of EL in the aorta and liver of apolipoprotein E knockout (EKO) mice was determined. EL in both mouse and rat liver was colocalized with vascular endothelial cells but not with hepatocytes. In contrast, HL was present in both hepatocytes and endothelial cells. By in situ hybridization, EL mRNA was present only in endothelial cells in liver sections. EL was also present at low levels in aorta of normal mice. We fed EKO mice and wild-type mice a variety of diets and determined EL expression in liver and aorta. EKO mice showed significant expression of EL in aorta. EL expression was lower in the liver of EKO mice than in normal mice. Cholesterol feeding decreased EL in liver of both types of mice. In the aorta, EL was higher in EKO than in wild-type mice, and cholesterol feeding had no effect. Together, these data suggest that EL may be upregulated at the site of atherosclerotic lesions and thus could supply lipids to the area.

Animals↗
PubMed1999

Coexpression of mineralocorticoid receptors and 11beta-hydroxysteroid dehydrogenase 2 in human gastric mucosa.

The role of mineralocorticoids in human gastrointestinal tract is well established. In the stomach, aldosterone is thought to regulate electrolyte transport associated with gastric acid secretion. In mineralocorticoid target organs, the action of the glucocorticoid inactivating enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) facilitates aldosterone binding to a nonselective mineralocorticoid receptor (MR) in the face of high levels of circulating glucocorticoids. In the present study, we examined 25 specimens of human stomach for the presence of MR and 11beta-HSD2 using a [3H]aldosterone binding assay, Northern blot analysis, RT-PCR, and immunohistochemistry. Specific [3H]aldosterone binding sites were detected in gastric fundic mucosa, but not in the antrum. In fundic mucosa the Kd was 0.72+/-0.05 nmol/L (mean +/- SE), and Bmax was 6.0+/-1.4 fmol per milligram of protein. Northern blot analysis demonstrated a faint band for MR mRNA at 6.0 kb, although message for 11beta-HSD2 was undetectable. However, RT-PCR demonstrated specific PCR products for both MR and 11beta-HSD2. Immunohistochemistry demonstrated the colocalization of MR and 11beta-HSD2 only in parietal cells. MR-positive cells were further characterized by electron microscopy, confirming the identity of parietal cells. This study shows that parietal cells contain both MR and 11beta-HSD2, suggesting that the human stomach is a novel target organ for mineralocorticoids. Aldosterone may, therefore, regulate biological functions of parietal cells including gastric acid secretion.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2006

Enhancement of anticancer activity in antineovascular therapy is based on the intratumoral distribution of the active targeting carrier for anticancer drugs.

We previously observed the enhanced anticancer efficacy of anticancer drugs encapsulated in Ala-Pro-Arg-Pro-Gly-polyethyleneglycol-modified liposome (APRPG-PEG-Lip) in tumor-bearing mice, since APRPG peptide was used as an active targeting tool to angiogenic endothelium. This modality, antineovascular therapy (ANET), aims to eradicate tumor cells indirectly through damaging angiogenic vessels. In the present study, we examined the in vivo trafficking of APRPG-PEG-Lip labeled with [2-(18)F]2-fluoro-2-deoxy-D-glucose ([2-(18)F]FDG) by use of positron emission tomography (PET), and observed that the trafficking of this liposome was quite similar to that of non-targeted long-circulating liposome (PEG-Lip). Then, histochemical analysis of intratumoral distribution of both liposomes was performed by use of fluorescence-labeled liposomes. In contrast to in vivo trafficking, intratumoral distribution of both types of liposomes was quite different: APRPG-PEG-Lip was colocalized with angiogenic endothelial cells that were immunohistochemically stained for CD31, although PEG-Lip was localized around the angiogenic vessels. These results strongly suggest that intratumoral distribution of drug carrier is much more important for therapeutic efficacy than the total accumulation of the anticancer drug in the tumor, and that active delivery of anticancer drugs to angiogenic vessels is useful for cancer treatment.

Animals↗
PubMed2004

Analysis of protein distribution in cartilage using immunofluorescence and laser confocal scanning microscopy.

Protein localization in cartilage sections by antibodies that specifically bind to epitopes of a protein is one of the most powerful technologies in modern cartilage research. Studies using two or more primary antibodies that recognize different protein epitopes allow the colocalization of different gene products in one cartilage section. In addition, specific histochemical stains help to visualize nuclear DNA, mitochondria, and other subcellular compartments. By these immunohistological methods, the distribution of proteins can be analyzed throughout different zones of articular cartilage. In particular, with the use of laser scanning confocal microscopy, subcellular localization of proteins can also be determined (i.e, nuclear, cytoplasmic, membrane-associated, and extracellular). Overall, immunohistochemical methods are fairly simple to handle, and the reagents required are inexpensive, with the exception of basic technical equipment (fluorescence microscope or confocal microscope). However, as with many methodologies, technical knowledge and experience is important to avoid and/or interpret either false-positive or false-negative results.

Animals↗
PubMed2002

The DNA-compacting protein DCP68 from soybean chloroplasts is ferredoxin:sulfite reductase and co-localizes with the organellar nucleoid.

The multiple copies of the chloroplast genome (plastome) are condensed and organized into nucleoids by a set of proteins. One of these, the DNA-binding protein DCP68 from soybean, has previously been shown to compact DNA and to inhibit DNA synthesis in vitro. N-terminal amino acid analysis and the absorption spectrum of the purified protein suggest that DCP68 is the siroheme protein sulfite reductase, a ferredoxin-dependent enzyme that participates in sulfur assimilation for cysteine and methionine biosynthesis. The in vivo association of this protein with chloroplast nucleoids was confirmed by immuno-colocalization with antibodies against sulfite reductase from Arabidopsis thaliana. These results suggest that DCP68 is a bifunctional chloroplast protein that participates in reductive sulfur assimilation and plays a role in organellar nucleoid organization. The fact that dephosphorylation by alkaline phosphatase affects the binding of purified DCP68 to DNA in vitro might be indicative of the way the interaction of the protein with the nucleoid is regulated in vivo.

Amino Acid Sequence↗
PubMed2000

Calcium imaging demonstrates colocalization of calcium influx and extrusion in fly photoreceptors.

During illumination, Ca(2+) enters fly photoreceptor cells through light-activated channels that are located in the rhabdomere, the compartment specialized for phototransduction. From the rhabdomere, Ca(2+) diffuses into the cell body. We visualize this process by rapidly imaging the fluorescence in a cross section of a photoreceptor cell injected with a fluorescent Ca(2+) indicator in vivo. The free Ca(2+) concentration in the rhabdomere shows a very fast and large transient shortly after light onset. The free Ca(2+) concentration in the cell body rises more slowly and displays a much smaller transient. After approximately 400 ms of light stimulation, the Ca(2+) concentration in both compartments reaches a steady state, indicating that thereafter an amount of Ca(2+), equivalent to the amount of Ca(2+) flowing into the cell, is extruded. Quantitative analysis demonstrates that during the steady state, the free Ca(2+) concentration in the rhabdomere and throughout the cell body is the same. This shows that Ca(2+) extrusion takes place very close to the location of Ca(2+) influx, the rhabdomere, because otherwise gradients in the steady-state distribution of Ca(2+) should be measured. The close colocalization of Ca(2+) influx and Ca(2+) extrusion ensures that, after turning off the light, Ca(2+) removal from the rhabdomere is faster than from the cell body. This is functionally significant because it ensures rapid dark adaptation.

Animals↗
PubMed2003

Two neuropeptides colocalized in a command-like neuron use distinct mechanisms to enhance its fast synaptic connection.

In many neurons more than one peptide is colocalized with a classical neurotransmitter. The functional consequence of such an arrangement has been rarely investigated. Here, within the feeding circuit of Aplysia, we investigate at a single synapse the actions of two modulatory neuropeptides that are present in a cholinergic interneuron. In combination with previous work, our study shows that the command-like neuron for feeding, CBI-2, contains two neuropeptides, feeding circuit activating peptide (FCAP) and cerebral peptide 2 (CP2). Previous studies showed that high-frequency prestimulation or repeated stimulation of CBI-2 increases the size of CBI-2 to B61/62 excitatory postsynaptic potentials (EPSPs) and shortens the latency of firing of neuron B61/62 in response to CBI-2 stimulation. We find that both FCAP and CP2 mimic these two effects. The variance method of quantal analysis indicates that FCAP increases the calculated quantal size (q) and CP2 increases the calculated quantal content (m) of EPSPs. Since the PSP amplitude represents the product of q and m, the joint action of the two peptides is expected to be cooperative. This observation suggests a possible functional implication for multiple neuropeptides colocalized with a classical neurotransmitter in one neuron.

Action Potentials↗
PubMed2006

Efficacy and antivascular effects of EphA2 reduction with an agonistic antibody in ovarian cancer.

BACKGROUND: EphA2 is an oncoprotein and tyrosine kinase receptor that is overexpressed in ovarian and many other cancers. We investigated the effects of reduced EphA2 levels on tumor growth and the tumor microenvironment in an orthotopic ovarian cancer model. METHODS: The effect of the EphA2-agonistic monoclonal antibody EA5, alone or in combination with paclitaxel, on the growth of ovarian cancer cells (SKOV3ip1, HeyA8, and HeyA8MDR [taxane-platinum resistant]) was determined in vitro and in vivo by immunoblotting, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, and immunohistochemical analysis. Expression of EphA2 and markers of angiogenesis (CD31, vascular endothelial growth factor [VEGF], and basic fibroblast growth factor), proliferation (proliferating cell nuclear antigen), and endothelial cell apoptosis (CD31-terminal deoxynucleotidyl transferase biotin-deoxyuridine triphosphate nick-end labeling colocalization) and phosphorylation of Src were analyzed by immunoblotting, immunohistochemistry, immunofluorescence, and in situ hybridization in tumors from treated mice. Statistical tests were two-sided. RESULTS: EA5 antibody treatment led to a more than 90% reduction in EphA2 expression in HeyA8 tumors in vivo. In mice bearing orthotopic SKOV3ip1 or HeyA8 tumors, 4 weeks of EA5 treatment resulted in tumors that weighed 31% and 45% less, respectively, than those in control (IgG-treated) mice (95% confidence interval [CI] = -0.09% to 71% and 20% to 70%, P = .27 and .01, respectively). Combination therapy with EA5 and paclitaxel reduced tumor weight by 77% and 80% (95% CI = 63% to 91% and 68% to 91%), respectively, compared with paclitaxel alone and by 92% and 88% (95% CI = 87% to 97% and 80% to 94%), respectively, compared with IgG alone. Combination therapy also reduced the weight of HeyA8MDR tumors by 47% (95% CI = 24% to 72%) compared with paclitaxel. Mice bearing SKOV3ip1 or HeyA8 tumors that were treated with combination therapy survived longer than those treated with paclitaxel alone (median survival = 144 versus 69 days and 46 versus 37 days, respectively). EA5-treated tumors had reduced microvascular density, proliferation, and VEGF protein and mRNA levels, with increased endothelial cell apoptosis. EphA2 was associated with Src, which was rapidly dephosphorylated after EA5 treatment. CONCLUSIONS: EA5 in combination with paclitaxel decreased tumor growth in an orthotopic ovarian cancer mouse model through antiangiogenic mechanisms associated with reduced levels of VEGF and phosphorylated Src. Humanized antibody constructs against EphA2 are worthy of future study.

Analysis of Variance↗
PubMed1996

Progesterone receptor immunoreactivity in aromatic L-amino acid decarboxylase-containing neurons of the guinea pig hypothalamus and preoptic area.

A double-labeling immunofluorescence procedure was used to determine whether progesterone receptor (PR)-immunoreactive (IR) neurons in the preoptic area and hypothalamus of female guinea pigs also contained aromatic L-amino acid decarboxylase (AADC), an enzyme involved in the synthesis of both catecholamines and serotonin. Immunostaining was performed on cryostat sections prepared from ovariectomized guinea pigs primed by estradiol to induce PR. The nuclear presence of PR was visualized by a red fluorescence while the AADC-containing perikarya showed a yellow-green fluorescence. The topographic distribution of AADC-IR neurons was investigated by using a specific antiserum obtained by immunization of rabbits with a recombinant protein beta-galactosidase-AADC in the two regions known to contain the densest populations of estradiol-induced PR-IR cells: the preoptic area and the mediobasal hypothalamus. The localization of PR-IR and AADC-IR cell populations showed considerable overlap in these areas, mainly in the medial and periventricular preoptic nuclei and in the arcuate nucleus. A quantitative analysis of double-labeled cells estimated that about 15% to 23% of AADC-IR cells in the preoptic area and about 11% to 21% of AADC-IR cells in the arcuate nucleus possessed PR. This colocalization persisted throughout the rostrocaudal extent of these areas and represented 3% to 9% of the population of PR-IR cells. These findings provide neuroanatomical evidence that a subset of AADC neurons is directly regulated by progesterone. The exact physiological role of this enzyme in target cells for progesterone is not understood. AADC may be involved in functions other than that for the synthesis of the classical neurotransmitters.

Animals↗
PubMed2004

Increased citrullinated glial fibrillary acidic protein in secondary progressive multiple sclerosis.

In this study, we demonstrate that grossly unaffected white matter from secondary progressive multiple sclerosis (SP-MS) patients is heavily citrullinated, as compared to normal white matter from control patients. Citrullination was most pronounced at plaque interfaces and was shown to colocalize with glial fibrillary acidic protein (GFAP)-immunoreactivity using dual color immunofluorescence. In contrast, the plaques themselves weakly stained for citrullinated proteins compared to control white matter and usually contained a blood vessel with surrounding astrocytes that were positive both for citrullinated proteins and GFAP. In SP-MS brain samples, but not in normal brains, long fibers of colocalized GFAP- and citrullinated proteins extended into the gray matter. Increased numbers of astrocytes containing citrullinated proteins and GFAP were also present at the junction between the gray and white matter in SP-MS brains. Western blot analysis of acidic brain proteins from nonplaque-containing white matter showed upregulation of multiple citrullinated GFAP proteins in SP-MS brains as compared to controls. Our results demonstrate that increased amounts of citrullinated GFAP are present in SP-MS brains, but also shows that these proteins are present in areas of MS brains that were grossly normal appearing. These data raise the possibility that citrullination of GFAP contributes to the pathophysiology of MS.

Adult↗
PubMed1992

Aberrant expression of the simple epithelial type II keratin 8 by mouse skin carcinomas but not papillomas.

Keratins have been demonstrated to be suitable markers of changes taking place during epithelial neoplasia. Therefore, we analyzed 18 mouse skin tumors (nine papillomas and nine squamous cell carcinomas), induced either by two-stage carcinogenesis with 7,12-dimethylbenz[a]anthracene(DMBA)/12-O-tetradecanoylphorbol-13-acetat e or complete carcinogenesis with DMBA, by immunofluorescence with a monoclonal antibody to keratin (K) 8 (TROMA-1). Immunoperoxidase staining and immunoblotting were also used on selected tumor samples to further explore for the presence of K8. All of the papillomas tested were negative for the presence of K8, whereas the carcinomas were positive. The level of K8 expression in carcinomas showed a positive correlation with the degree of malignancy. Northern blot analysis using a K8 cDNA probe suggested that control of K8 expression in mouse skin tumors occurs at the transcriptional level. Double-label immunofluorescence staining using TROMA-1 and RK13 antibodies demonstrated that K8 did not generally colocalize with K13, a keratin normally found in internal stratified epithelial but aberrantly expressed in mouse epidermal tumors. Furthermore, tumors expressing high levels of K8 showed a reduced expression of K13. Histological examination of immunoperoxidase-stained tumors demonstrated that K8-positive cells were mainly found in anaplastic areas, whereas K13 foci were restricted to well-differentiated regions. Our results demonstrate that K8 expression is a marker of late stages of carcinoma progression in the mouse skin carcinogenesis model.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2000

Occludin localization at the tight junction requires the second extracellular loop.

Occludin is a transmembrane protein of the tight junction with two extracellular loops. Our previous demonstration that the extracellular loops are adhesive suggested the possibility that they contribute to localizing occludin at the tight junction. To address this question, truncated forms of occludin were generated in which one or both of the extracellular loops were deleted. These constructs were expressed in both occludin-null Rat-1 fibroblasts and in MDCK epithelial cells. The patterns of sensitivity to proteinase K suggested all constructs were present on the plasma membrane and retained the normal topology. In fibroblasts, all truncated forms of occludin colocalized with ZO-1 at regions of cell-cell contact, demonstrating that even in the absence of tight junctions cytoplasmic interactions with ZOs is sufficient to cluster occludin. In MDCK cell monolayers, both full-length and occludin lacking the first extracellular loop colocalized with ZO-1 at the tight junction. In contrast, constructs lacking the second, or both, extracellular loops were absent from tight junctions and were found only on the basolateral cell surface. By freeze-fracture electron microscopic analysis, overexpression of full length occludin induced side-to-side aggregation of fibrils within the junction, while excess occludin on the lateral membrane did not form fibrils. These results suggest that the second extracellular domain is required for stable assembly of occludin in the tight junction and that occludin influences the structural organization of the paracellular barrier.

Animals↗
PubMed2005

Interaction of transducin-alpha with LGN, a G-protein modulator expressed in photoreceptor cells.

LGN and activator of G-protein signaling 3 (AGS3) belong to the class of G-protein modulators containing G-protein regulatory motifs (GPR proteins). Evidence for the functions of these molecules has only started to emerge. Immunostaining of mouse retina cross-sections and serial tangential sectioning of the retina combined with immunoblot analysis revealed that LGN is expressed in the inner segments of photoreceptor cells. Double immunolabeling demonstrated that, following light-dependent translocation from the outer segments, the alpha-subunit of the visual G-protein transducin (Gtalpha) colocalizes with LGN in the basal part of the inner segments. LGN and Gtalpha coprecipitate from the retinal extracts, supporting the notion of the interaction between the proteins. Furthermore, the GPR domain of LGN potently inhibits receptor-mediated guanine nucleotide exchange and steady-state GTPase activity of transducin. The localization and interaction with Gtalpha suggest LGN roles in modulation of transducin translocation and other photoreceptor cell functions.

Animals↗
PubMed2004

Novel human testis-specific histone H2B encoded by the interrupted gene on the X chromosome.

Testis-specific histones are synthesized and accumulated at specific stages of mammalian spermatogenesis. Their proposed functions range from facilitation of the replacement of somatic histones by protamines to epigenetic control of gene transcription. Several testis histone variants were characterized in mouse and rat; however, few are known in humans. Here we report the identification and characterization of a novel human histone 2B gene (TH2B-175) located at Xq22.2, which encodes a highly divergent H2B variant. The TH2B-175 gene contains two introns and is transcribed exclusively in testis, where the spliced polyadenylated mRNA was detected. Genomic PCR, Southern blot analysis, and BLAST-based searches indicate that TH2B-175 evolved in the primate lineage or has been lost in rodents. In transfected Chinese hamster cells, GFP-tagged TH2B-175 targeted to large fluorescent bodies that partially colocalize with the interstitial telomeric blocks. Therefore, TH2B-175 may have telomere-associated functions and participate in the telomere-binding complex in the human sperm [1].

Alternative Splicing↗
PubMed2000

The recruitment of the interleukin-1 (IL-1) receptor-associated kinase (IRAK) into focal adhesion complexes is required for IL-1beta -induced ERK activation.

The interleukin-1 (IL-1) receptor colocalizes with focal adhesion complexes (FACs), actin-enriched structures involved in cell adhesion and signaling in fibroblasts and chondrocytes. The colocalization of FACs and IL-1 receptors has been implicated in the restriction of IL-1 signaling transduction to ERK; however, the mechanism of this restriction and the requirement of IL-1 receptor-associated proteins have not been characterized. We determined if the association kinetics of the interleukin-1 receptor-associated kinase (IRAK) colocalizes with FACs and the requirement for IRAK in IL-1-dependent ERK activation. Human gingival fibroblasts were incubated with collagen-coated beads to induce the assembly of FACs at sites of cell-bead contact. Immunoblot analysis of bead-isolated FACs showed a time-dependent assembly of the focal adhesion proteins beta-actin, vinculin, and talin, which was blocked by the actin monomer sequestering toxin latrunculin B. Although no IRAK was isolated with FACs from unstimulated cells, phosphorylated IRAK was transiently associated with FACs isolated from IL-1beta-stimulated fibroblasts. Fibroblasts plated on tissue culture plastic (which permitted the formation of focal adhesions) showed phosphorylation of ERK, JNK, and p38. Cells plated on poly-l-lysine (to prevent the formation of focal adhesions) showed activation only of JNK and p38. ERK activation was partially restored by incubating cells plated on poly-l-lysine with collagen-coated beads before IL-1 stimulation. Cells treated with latrunculin B or swinholide A, which caused a progressive depolymerization of actin filaments, showed a reduction or elimination of IL-1-induced ERK activation, respectively. Fibroblasts electroinjected with a mouse monoclonal anti-IRAK antibody to block the recruitment of IRAK into FACs failed to activate ERK after IL-1 treatment, indicating that FAC-associated IRAK is required for the activation of ERK. These data indicate that the integrity of actin filament arrays and the recruitment of IRAK into focal adhesions are involved in the restriction of IL-1 signaling to ERK.

Actins↗
PubMed2000

Characterization of the interaction between protein 4.1R and ZO-2. A possible link between the tight junction and the actin cytoskeleton.

Multiple isoforms of the red cell protein 4.1R are expressed in nonerythroid cells, including novel 135-kDa isoforms. Using a yeast two-hybrid system, immunocolocalization, immunoprecipitation, and in vitro binding studies, we found that two 4.1R isoforms of 135 and 150 kDa specifically interact with the protein ZO-2 (zonula occludens-2). 4.1R is colocalized with ZO-2 and occludin at Madin-Darby canine kidney (MDCK) cell tight junctions. Both isoforms of 4.1R coprecipitated with proteins that organize tight junctions such as ZO-2, ZO-1, and occludin. Western blot analysis also revealed the presence of actin and alpha-spectrin in these immunoprecipitates. Association of 4.1R isoforms with these tight junction and cytoskeletal proteins was found to be specific for the tight junction and was not seen in nonconfluent MDCK cells. The amino acid residues that sustain the interaction between 4.1R and ZO-2 reside within the amino acids encoded by exons 19-21 of 4.1R and residues 1054-1118 of ZO-2. Exogenously expressed 4.1R containing the spectrin/actin- and ZO-2-binding domains was recruited to tight junctions in confluent MDCK cells. Taken together, our results suggest that 4.1R might play an important role in organization and function of the tight junction by establishing a link between the tight junction and the actin cytoskeleton.

Actins↗
PubMed1999

Accumulation of amyloid beta and tau and the formation of neurofilament inclusions following diffuse brain injury in the pig.

Brain trauma in humans increases the risk for developing Alzheimer disease (AD) and may induce the acute formation of AD-like plaques containing amyloid beta (A beta). To further explore the potential link between brain trauma and neurodegeneration, we conducted neuropathological studies using a pig model of diffuse brain injury. Brain injury was induced in anesthetized animals via nonimpact head rotational acceleration of 110 degrees over 20 ms in the coronal plane (n = 15 injured, n = 3 noninjured). At 1, 3, 7, and 10 days post-trauma, control and injured animals were euthanized and immunohistochemical analysis was performed on brain sections using antibodies specific for A beta, beta-amyloid precursor protein (betaPP), tau, and neurofilament (NF) proteins. In addition to diffuse axonal pathology, we detected accumulation of A beta and tau that colocalized with immunoreactive betaPP and NF in damaged axons throughout the white matter in all injured animals at 3-10 days post-trauma. In a subset of brain injured animals, diffuse A beta-containing plaque-like profiles were found in both the gray and white matter, and accumulations of tau and NF rich inclusions were observed in neuronal perikarya. These results show that this pig model of diffuse brain injury is characterized by accumulations of proteins that also form pathological aggregates in AD and related neurodegenerative diseases.

Amyloid beta-Peptides↗
PubMed2004

The herpesvirus saimiri ORF73 gene product interacts with host-cell mitotic chromosomes and self-associates via its C terminus.

The herpesvirus saimiri (HVS) ORF73 gene product shares limited homology with the ORF73 protein of Kaposi's sarcoma-associated herpesvirus (KSHV). ORF73 is expressed in an in vitro model of HVS latency, where the genome persists as a non-integrated circular episome. This suggests it may have a similar role to KSHV ORF73 in episomal maintenance, by tethering viral genomes to host-cell chromosomes. Here, the association of ORF73 with host mitotic chromosomes is described. Deletion analysis demonstrates that the distal 123 aa of the ORF73 protein are required for mitotic chromosomal localization and for self-association. Moreover, deletion of the extreme C terminus disrupts both self-association and host mitotic chromosome colocalization. This suggests that HVS ORF73 has a similar role to KSHV ORF73 in episomal maintenance and that association of ORF73 to host mitotic chromosomes is dependent on its ability to form multimers.

Amino Acid Sequence↗