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PubMed2001

Ectopic sequences from truncated HMGIC in liposarcomas are derived from various amplified chromosomal regions.

The HMGIC gene codes for an architectural transcription factor frequently rearranged by translocation in lipomas and other benign mesenchymal tumors. In sarcomas, malignant tumors of mesenchymal origin, the gene is also found to be rearranged, but in addition amplified and overexpressed. Here we report the sequence, chromosomal localization, and expression patterns of 11 novel ectopic sequences fused to exons 2 and 3 of HMGIC in seven different sarcoma samples. In addition, we identified a number of variant transcripts observed previously in benign tumors. Consistent with the suggested role of HMGIC in adipocytic differentiation, most of the novel ectopic sequences were observed in well-differentiated liposarcomas. These tumors are known to have complex marker chromosomes containing amplified segments from several chromosomes. Five novel sequences were derived from 12q14-q15, where HMGIC resides, two from 1q24, a region frequently amplified in these types of tumors, two from 11q14, and one from chromosome 2. All except one of the aberrant transcripts encoded truncated proteins with intact DNA-binding domains (AT hooks) but lacking the C-terminal acidic region, a target for constitutive phosphorylation by protein kinase CK2. Some of the ectopic sequences were transcribed in other tissues, and most of the ectopic sequences also showed recurrent amplification in liposarcomas.

Amino Acid Sequence↗
PubMed1994

Differentiation ability and oncogenic potential of HPV-33- and HPV-33 + ras-transfected keratinocytes.

Five HPV-33-immortalized and 5 HPV-33 + ras-transfected cell lines were characterized in terms of growth in soft agar, tumorigenic potential in nude mice, p21 expression, morphology and expression of differentiation markers in organotypic cultures. No striking differences were observed between the HPV-33-immortalized cell lines and their corresponding ras-transfected counterparts as regards their tumorigenicity in nude mice (only one cell line was able to develop tumors in nude mice) or their behavior on lifted collagen gels. However, all the ras-transfected cell lines gave rise to colonies in soft agar while only 2 HPV-33-transfected lines (CK1 and CK4) displayed this property. The 10 cell lines could be divided into 2 groups with respect to their phenotype in monolayer and in organotypic cultures. Lines from group I (CK2, 3, 5 and their ras-transfected homologous lines) shared a typical epithelial phenotype in monolayer and the ability (a) to form an epithelium similar to a CIN-III lesion and (b) to strongly express keratins K1-K10 and involucrin in organotypic cultures. On the other hand, for the lines from group II (CK1, CK4, CK1EJ7 and CK4EJ5), there was a correlation between an elongated phenotype in monolayer and the property (a) to form a structure similar to a microinvasive carcinoma and (b) to express vimentin and keratins K8-K18. These cell lines, exhibiting various transformation-associated alterations, can be considered as an in vitro model representing various stages of HPV-33-associated cervical carcinogenesis.

Animals↗
PubMed1982

Monoclonal cytokeratin antibodies that distinguish simple from stratified squamous epithelia: characterization on human tissues.

Four monoclonal antibodies designated CK1 - CK4 were obtained from fusions of mouse myeloma F0 cells with spleen cells from BALB/c mice immunized with cytoskeletal preparations made by treatment of human HeLa cells with non-ionic detergents. These IgG1 type antibodies all recognize, in immune blots, cytokeratin 18 (45 kd, pI 5.7) in the catalogue of 19 human cytokeratin species developed by Moll et al. (1982). Immunofluorescence microscopy on human material shows that CK1 - CK4 stain a wide variety of simple epithelia (e.g., intestine, respiratory and urinary systems, liver, glandular epithelia) but do not stain stratified squamous epithelia (e.g., oesophagus, epidermis) or non-epithelial cells. The immunofluorescence results, developed mainly by gel electrophoresis, support the concept of cytokeratin divergence in different epithelia and clarify, for cytokeratin 18, some unsolved problems posed by high tissue complexity. CK2 appears specific for human, CK1 and CK3 for primates, while CK4 shows broad cross-species reactivity. Thus, CK1 - CK4 appear to be valuable tools for cytokeratin typing and initial experiments also suggest that they can be used to further subdivide human tumours of epithelial origin.

Animals↗
PubMed1984

Tissue polypeptide antigen (TPA) is related to the non-epidermal keratins 8, 18 and 19 typical of simple and non-squamous epithelia: re-evaluation of a human tumor marker.

Because of the broad clinical interest which tissue polypeptide antigen (TPA) has attracted as a tumor marker, human cell lines and human tissues have been analyzed for TPA expression using immunofluorescence microscopy. Epithelial cell lines including HeLa, MCF-7, and A-431 are recognized by TPA antibodies whereas human lines of non-epithelial origin are not. The positive staining patterns coincide with keratin-type intermediate filaments of the cytoskeleton. On tissue sections a subset of epithelial cells including uterine epithelium, bile duct cells in liver and tumor cells in breast carcinoma are strongly positive; cells of the squamous epithelia of skin and tongue as well as cells of non-epithelial origin are negative. In immunoblots of human epidermis, human tongue mucosa, human hair follicles, Detroit 562 cells, HeLa cells, MCF-7 and RT-4 cells, only keratins 8, 18 and 19 show TPA antigenicity. Conversely a TPA preparation is recognized by various antibodies known to react with keratins, including alpha-IFA, KG 8.13.2 and two antibodies which recognize keratins 18 (CK2) and 19, respectively. Our results thus relate TPA to human keratins 8, 18 and 19 which are known cytoskeletal components in both normal and malignant epithelial cells of simple and non-squamous origin. We speculate that the elevated levels of circulating TPA antigenicity present in the sera of patients with carcinoma, which are often used to monitor tumor progression, correspond to soluble proteolytic fragments originating from this particular keratin subgroup.

Animals↗
PubMed2004

Increased expression of the MBP mRNA binding protein HnRNP A2 during oligodendrocyte differentiation.

Heterogeneous nuclear ribonucleoprotein (hnRNP) A2, a trans-acting factor that mediates intracellular trafficking of myelin basic protein (MBP) mRNA to the myelin compartment in oligodendrocytes, is most abundant in the nucleus, but shuttles between the nucleus and cytoplasm. In the cytoplasm, it is associated with granules that transport mRNA from the cell body to the processes of oligodendrocytes. We found that the overall level of hnRNP A2 increased in oligodendrocytes as they differentiated into MBP-positive cells, and that this augmentation was reflected primarily in the cytoplasmic pool of hnRNP A2 present in the form of granules. The extranuclear distribution of hnRNP A2 was also observed in brain during the period of myelination in vivo. Methylation and phosphorylation have been implicated previously in the nuclear to cytoplasmic distribution of hnRNPs, so we used drugs that block methylation and phosphorylation of hnRNPs to assess their effect on hnRNP A2 distribution and mRNA trafficking. Cultures treated with adenosine dialdehyde (AdOx), an inhibitor of S-adenosyl-L-homocysteine hydrolase, or with 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), a drug that inhibits casein kinase 2 (CK2), maintained the preferential nuclear distribution of hnRNP A2. Treatment with either drug affected the transport of RNA trafficking granules that remained confined to the cell body.

Animals↗
PubMed2003

Changes in gene expression during chemical-induced nephrocarcinogenicity in the Eker rat.

Hydroquinone (HQ) is a rodent carcinogen and a potential human carcinogen. Glutathione conjugation of HQ enhances its biological reactivity, and 2,3,5-tris-(glutathion-S-yl)hydroquinone (TGHQ) is a potent nephrotoxicant and nephrocarcinogen in the Eker rat. Moreover, a single exposure of primary epithelial cells derived from Eker rat kidneys to TGHQ transforms these cells into an immortalized phenotype (quinol-thioether transformed rat renal epithelial (QT-RRE) cells). The Eker rat bears a mutation in one allele of the tuberous sclerosis-2 (Tsc-2) tumor suppressor gene, which predisposes the animals to the development of spontaneous and chemical-induced renal cell carcinoma. Thus, the Eker rat provides a unique model for elucidating the mechanisms of renal tubular epithelial carcinogeneisis. cDNA microarray analysis of QT-RRE3 cells and of tumor tissue derived from the kidneys of Eker rats treated with TGHQ revealed alterations (by threefold or greater) in the expression of a total of 80 genes. Fifteen percent of these genes exhibited similar expression patterns in both QT-RRE cells and tumor tissue. The differentially expressed genes primarily participate in three major areas: (1) signal transduction or in the regulation of signal transduction (extracellular signal regulated kinase 2 (ERK2); protein kinase CK2; protein kinase B; c-jun; NF-kappaB; ras-related GTPases; annexins), (2) stress response, tissue remodeling, and DNA repair (glutathione-S-transferases; procollagen c proteinase enhancer; plasminogen activator; tissue inhibitor of metalloprotease 3; apurinic/apyrimidic endonuclease), and (3) electron transport and energy homeostasis (cytochrome c oxidase subunits). The changes in the expression of many of these genes was confirmed by reverse transcription (RT)-polymerase chain reactions (PCR) using primers specific for the differentially expressed genes. As an example, the annexin I and II genes, implicated in signal transduction, were highly induced in tumor tissue and also in dysplastic lesions isolated from the kidneys of rats treated chronically with TGHQ. The annexin I and II proteins were also upregulated in tumor tissue, which probably play an important role in TGHQ-induced nephrocarcinogenesis. Moreover, in the present study, a tumorigenicity assay using athymic nude mice revealed that QT-RRE cell lines formed tumors when injected in the subcutis of nude mice, providing evidence that the cells are malignantly transformed. Histopathological analysis further indicated that the tumors were composed of neoplastic cells, resembling renal carcinoma cells with varying degrees of atypia, with the presence of apoptotic and mitotic figures.

Animals↗
PubMed2006

Arsenite inhibits p53 phosphorylation, DNA binding activity, and p53 target gene p21 expression in mouse epidermal JB6 cells.

Epidemiologic investigations demonstrated that arsenite exposure increases the risk of various human cancers, including skin, lung, bladder, and kidney cancers. However, oral administration of arsenite alone has failed to induce tumors in animal models, suggesting that arsenic may act to enhance mutagenicity induced by other carcinogens. Arsenite may function as a co-carcinogen, acting by inhibiting repair of carcinogen-induced DNA damage mediated by p53 and p21, a p53 target gene. To elucidate the interaction between arsenite and p53 tumor suppressor protein, we studied the effect of arsenite on ultraviolet B (UVB)-induced p53 phosphorylation, p53 DNA binding activity, and p53-induced target gene transactivation in the JB6 Cl41 mouse epidermal skin cell model. Our results indicated that arsenite suppressed UVB-induced p53 phosphorylation and p53 DNA binding activity. Arsenite also inhibited casein kinase 2 (CK2) activity and decreased p53-regulated p21 protein expression. These data suggest that the direct inhibition of p53 functional activation is one of the mechanisms through which arsenite interferes with p53 function, and thus may be a significant mechanism for the co-carcinogenic effects of arsenite.

Animals↗
PubMed2003

Spermatogenesis of mice lacking CK2alpha': failure of germ cell survival and characteristic modifications of the spermatid nucleus.

Csnk2a2 encodes the CK2alpha'catalytic subunit of CK2 that is predominantly expressed in testis. Male mice in which Csnk2a2 has been disrupted were infertile and displayed oligozoospermia with an abnormal shape of the spermatid nucleus. In this study, Csnk2a2 null testes revealed extensive germ cell degenerative processes at all stages of spermatogenesis, including the first spermatogenesis wave. Nuclear envelope (NE) protrusions with loss of nuclear pores, swelling of the outer membrane, and disruption of the inner membrane were observed in cells ranging from spermatogonia to early spermatids. Most early round spermatids were depleted, and DNA-specific fluorescent dyes showed a large chromatin-free nuclear domain near the chromocenter. Spermatids that were not eliminated retained NE defects that could explain the acrosomal and nuclear abnormalities of Csnk2a2 null spermatozoa. Data suggest that CK2alpha' deficiency could impair the phosphorylation of nuclear proteins of male germ cells leading to a particular cell-death pathway characterized by NE protrusions and an unusual pattern of chromatin modifications in spermatids.

Animals↗
PubMed1998

Molecular identification and expression of erythroid K:Cl cotransporter in human and mouse erythroleukemic cells.

A major pathway for K+ efflux in human reticulocytes and young RBCs is K:Cl cotransport (K:Cl-CT). The activity of K:Cl-CT is increased in pathologic RBCs containing hemoglobins S and C and may contribute to the abnormal dehydration state of these cells. Human K:Cl-CT (gene product KCC1) has been recently sequenced from human (hKCC1), rabbit and rat tissue by Gillen et al. (J Biol Chem 271:16237, 1996). We report here the sequence of KCC1 from human and mouse erythroleukemic cells (K562 and MEL cells, respectively). The cDNA for human erythroid-KCC1 is 100% identical to hKCC1 and the cDNA for mouse erythroid-KCC1 shares 89% identity with hKCC1, which translates to 96% identity at the amino acid level. Mammalian KCC1 is strongly conserved with >95% identity between human, rabbit, rat, and mouse KCC1 proteins. We did not detect any full-length mRNA transcripts of human erythroid-KCC1 in circulating reticulocytes. We detected two mRNA isoforms of human erythroid-KCC1 that resulted in C-terminal truncated proteins (73 amino acid and 17 amino acids, respectively). Human and mouse erythroidKCC1 differed at several consensus sites including a predicted PKC phosphorylation site at 108threonine and a predicted CK2 phosphorylation site at 51serine, within the predicted cytoplasmic N-terminal, that are present in human but not mouse erythroid-KCC1. Expression of MEL-KCC1 mRNA increases substantially upon DMSO-induced differentiation opening the possibility that erythroid-KCC1 plays a role in early erythroid maturation events. The molecular identification of erythroid-KCC1 is an important step towards understanding the physiologic role mediated by this protein in young and pathologic RBCs and during erythropoiesis, as well as providing a new tool for the elucidation of pathways and signals involved in RBC volume regulation.

Amino Acid Sequence↗
PubMed1998

Molecular cloning and characterization of ZNF202: a new gene at 11q23.3 encoding testis-specific zinc finger proteins.

Two distinct regions of loss of heterozygosity (LOH) in breast carcinomas were previously identified at chromosome 11q23. With the aim of identifying a tumor suppressor gene, we undertook the isolation and characterization of genes within LOH region 2, defined between loci D11S1345 and D11S1316, which spans an area of about 1 Mb. Here, we describe the cloning and characterization of a new gene, ZNF202. The gene, which spans a genomic area of approximately 10 kb, is almost exclusively expressed in testis as a 4-kb mRNA. The predicted amino acid sequence of the protein product revealed significant homologies with zinc finger proteins, indicating that the ANF202 protein may function as a transcription factor. The presence of multiple CK2 and PKC phosphorylation sites suggests that its activity may be regulated by phosphorylation. The gene is also expressed in breast carcinoma cell lines. However, mutation analysis of 39 breast cancer samples revealed no evidence of mutations, indicating that ZNF202 is unlikely to be involved in the pathogenesis of this neoplasm. Nevertheless, a role for ZNF202 in the tumorigenic process of other tissues cannot be excluded.

Amino Acid Sequence↗
PubMed2003

Estrogen receptor expression profile of disseminated epithelial tumor cells in bone marrow of breast cancer patients.

The estrogen receptor (ER) status in primary breast cancer represents an important prognostic factor and has a profound impact on therapeutic decisions. However, ER expression profile on disseminated breast cancer cells is largely unknown, although these cells are one of the main target structures in adjuvant therapy after local curative resection (R0) achieved in most breast cancer patients. Thus, the present pilot study was designed to evaluate the ER expression profile on disseminated epithelial cells in bone marrow, one of the preferential organs for manifestation of distant metastases in breast cancer. Using the alkaline phosphatase anti-alkaline phosphatase-immunogold double staining procedure, in a panel of 17 breast cancer patients, epithelial cells (mab CK2) detected in bone marrow were analyzed for ER expression (mab 1D5) and compared with ER expression in the corresponding primary tumors. Whereas eleven of the 17 patients (64.7%) were ER-positive in primary carcinomas, only two patients (11.8%) revealed ER-positive epithelial cells in bone marrow. In addition, one of these two patients demonstrated a heterogeneous ER expression pattern, with both ER-positive and ER-negative epithelial cells in bone marrow. Although in both of these cases the ER-positive epithelial cells in bone marrow derived from ER-positive primary tumors, in this small patient cohort none of the prognostic relevant clinical and pathological factors tested, i.e., TNM-classification, grading, and ER status in primary breast cancer, correlated with the ER status in bone marrow. The striking discrepancy between ER expression in primary breast cancers and the corresponding disseminated epithelial cells in bone marrow suggests either the selective dissemination of ER-negative tumor cells into the bone marrow or a negative impact of the bone marrow microenvironment on epithelial ER expression. This phenomenon might influence therapeutic effects of antihormonal treatment.

Bone Marrow↗
PubMed2003

Minimal residual disease in gastric cancer.

In curatively resected gastric cancer, the incidence of distant relapse is as high as 30%. Although the most important factor contributing to the local control of the tumor is the microscopic tumor-free margin of the surgical resection, the occurrence of distant metastases is in many cases due to preoperative or perioperative tumor cell dissemination. In addition to the established TNM staging system, disseminated tumor cells may serve as independent prognostic factors influencing patient outcome after curative surgery. Basically, in gastric cancer three compartments have been identified in which single tumor cells may be shed: lymph nodes, peritoneal cavity, and bone marrow. Assessment of resected regional lymph nodes with monoclonal antibodies directed against cytokeratin antigens leads to an upstaging in comparison with conventional histology. Nodal micrometastases detected by immunohistochemistry result in an upstaging of up to 36% of patients. However, their prognostic significance remains controversial. Local dissemination of tumor cells in the peritoneal cavity determines the outcome in advanced gastric cancer and diffuse-type carcinoma. Patients with negative peritoneal washings seem to have a more favorable prognosis. Moreover, with the use of these diagnostic tools, patient subpopulations may be identified which profit from intraperitoneal therapy regimens. Diffuse hematogenous tumor cell dissemination into the bone marrow has been shown to be a prognostic factor in several studies. In our own population of 180 gastric cancer patients, bone marrow cells were screened immunohistochemically with a monoclonal antibody directed against cytokeratin 18 (CK18). In 95 patients (53%), CK2-posititve cells were detected. In a multivariate analysis, the independence of the presence of three or more disseminated tumor cells per 10(6) mononuclear cells was proven to be a prognostic factor in patients with intestinal-type tumors, pT1/2 status, and pN0 status. In conclusion, the TNM status only partially reflects the actual extent of systemic disease in patients with resected gastric cancer. The assessment of minimal residual disease is valuable in estimating the prognosis in many patients. In the future, staging systems will have to not only include TNM data but also provide specific information on biological properties of residual cancer cells in order to establish more exact prognostic estimates and provide patients with an individually tailored multimodal treatment.

Bone Marrow Neoplasms↗
PubMed1996

[Tumor cell dissemination in bone marrow and peritoneal cavity. An immunocytochemical study of patients with stomach or colorectal carcinoma].

The tumor spread and the radicality of surgical resection are the most important facts in a patient's prognosis. In spite of curative tumor resection many patients die from metastases or local tumor recurrence. One possible reason is early dissemination of tumor cells which cannot be detected with clinical methods of examination. For this reason the aim of our study was to examine both bone marrow and peritoneal lavage for disseminated tumor cells with an immunocytochemical technique in patients with a gastrointestinal carcinoma. We also wanted to find out whether there was any correlation between the incidence of tumor cell detection and the TNM classification, staging and tumor grading and whether disseminated tumor cells have any prognostic significance. Our study included 54 patients who underwent surgery in our clinic for a carcinoma of the stomach (20 patients) or the colorectum (34 patients) from November 1993 to December 1994. At the beginning of the operation bone marrow had been taken from the iliac spine, and the abdomen was irrigated with 1000 ml saline solution immediately after laparotomy or laparoscopy. After cell separation with Ficoll density centrifugation 5 x 10(5) cells were applied per slide by a cytospin technique. For detection of the tumor cells we used the APAAP technique and the following monoclonal antibodies: KL1, CK2, anti-CEA, 17-1A (bone marrow) and Ber-EP4, B72.3, anti-CEA and 17-1A (peritoneal lavage). Altogether 77% of all patients had tumor cells in the bone marrow and 69% in peritoneal lavage fluid. It was possible to detect tumor cells in bone marrow (67%) and peritoneal lavage fluid (25%) even of patients with T1 tumors. The percentage increased with depth of wall infiltration. There was a marked difference in bone marrow aspirates between patients with lymph-node-negative tumors (N0) and those with lymph-node-positive tumors (N+): 65% had tumor cells in N0 and 85% in N+ stages. This trend was also seen in patients with (M1) and without (M0) metastases, in both bone marrow aspirates and peritoneal lavage fluid. In bone marrow there was a good correlation of tumor cells with staging, but in peritoneal lavage fluid this was not so. Finally, we detected tumor cells more often in bone marrow and peritoneal lavage fluid of patients with poorly differentiated tumors (G3) or diffuse Lauren type than in patients with moderately differentiated tumors (G2) or intestinal Lauren type. After a median follow-up period of 12.5 months patients with disseminated tumor cells had a lower survival rate than patients without tumor cells.

Adult↗
PubMed1993

Immunocytochemical double staining of cytokeratin and prostate specific antigen in individual prostatic tumour cells.

Early dissemination of malignant cells is the main cause for metastatic relapse in patients with solid tumours. By use of monoclonal antibodies (mAbs) specific for cytokeratins, disseminated individual epithelial tumour cells can now be identified in mesenchymal organs such as bone marrow. Further to characterize such cells in patients with prostate cancer, an immunocytochemical procedure was developed for simultaneous labelling of cytokeratin component no. 18 (CK18) and prostate specific antigen (PSA). In a first step, cells were incubated with mAb ER-PR8 against PSA and secondary gold-conjugated goat anti-mouse antibodies. In a second step, biotinylated mAb CK2 to CK18 was applied as primary antibody and subsequently incubated with complexes of streptavidin-conjugated alkaline phosphatase, which were developed with the Newfuchsin substrate. The binding of gold-labelled antibodies was visualized by silver enhancement. The sensitivity and specificity of the technique was demonstrated on cryostat sections of hyperplastic prostatic tissue, and cytological preparations of LNCaP prostatic tumour cells. Double staining was restricted to cells derived from the secretory epithelium of the prostate. Cross-reactivity between both detection systems was excluded by several controls, including the use of unrelated antibodies of the same isotype and the staining of CK18+/PSA- HT29 colon carcinoma cells. CK18+ cells co-expressing PSA were found in bone marrow aspirates from 5 out of 13 patients with carcinomas of the prostate, a finding that is consistent with the relative fraction of double-positive LNCaP cells. The specificity of CK18 for epithelial tumour cells in bone marrow was supported by negative staining of 12 control aspirates from patients with benign prostatic hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1995

Differential phosphorylation of MAP1b during postnatal development of the cat brain.

Microtubule-associated protein 1b, previously also referred to as microtubule-associated protein 5 or microtubule-associated protein 1x, is a major component of the juvenile cytoskeleton, and is essential during the early differentiation of neurons. It is required for axonal growth and its function is influenced by phosphorylation. The distribution of microtubule-associated protein 1b in kitten cerebellum and cortex during postnatal development was studied with two monoclonal antibodies. Hybridoma clone AA6 detected a non-phosphorylated site, while clone 125 detected a site phosphorylated by casein-kinase II. On blots, both monoclonal antibodies stained the same two proteins of similar molecular weights, also referred to as microtubule-associated protein 5a and 5b. Antibody 125 detected a phosphorylated epitope on both microtubule-associated protein 1b forms; dephosphorylation by alkaline phosphatase abolished the immunological detection. During development of cat cortex and cerebellum, AA6 stained the perikarya and dendrites of neurons during their early differentiation, and especially labelled newly generated axons. The staining decreased during development, and axonal staining was reduced in adult tissue. In contrast to previous reports which demonstrated that antibodies against phosphorylated microtubule-associated protein 1b label exclusively axons, antibody 125 also localized microtubule-associated protein 1b in cell bodies and dendrites, even in adulthood. Some nuclear staining was observed, indicating that a phosphorylated form of microtubule-associated protein 1b may participate in nuclear function. These results demonstrate that microtubule-associated protein 1b is subject to CK2-type phosphorylation throughout neuronal maturation and suggest that phosphorylation of microtubule-associated protein 1b may participate in juvenile and mature-type microtubule functions throughout development.

Animals↗
PubMed1998

Nucleotide and deduced amino acid sequences of rat myosin binding protein H (MyBP-H).

The complete nucleotide sequence of the cDNA clone encoding rat skeletal muscle myosin-binding protein H (MyBP-H) was determined and amino acid sequence was deduced from the nucleotide sequence (GenBank accession number AF077338). The full-length cDNA of 1782 base pairs(bp) contains a single open reading frame of 1454 bp encoding a rat MyBP-H protein of the predicted molecular mass 52.7 kDa and includes the common consensus 'CA__TG' protein binding motif. The cDNA sequence of rat MyBP-H show 92%, 84% and 41% homology with those of mouse, human and chicken, respectively. The protein contains tandem internal motifs array (-FN III-Ig C2-FN III-Ig C2-) in the C-terminal region which resembles to the immunoglobulin superfamily C2 and fibronectin type III motifs. The amino acid sequence of the C-terminal Ig C2 was highly conserved among MyBPs family and other thick filament binding proteins, suggesting that the C-terminal Ig C2 might play an important role in its function. All proteins belonging to MyBP-H member contains 'RKPS' sequence which is assumed to be cAMP- and cGMP-dependent protein kinase A phosphorylation site. Computer analysis of the primary sequence of rat MyBP-H predicted 11 protein kinase C (PKC) phosphorylation site, 7 casein kinase II (CK2) phosphorylation site and 4 N-myristoylation site.

Amino Acid Sequence↗
PubMed2005

Cyclin H is targeted to the nucleus by C-terminal nuclear localization sequences.

Cdk-activating kinase (CAK) is a trimeric complex consisting of cdk7, cyclin H, and MAT1, which activates the cell-cycle-regulating cdks through T loop phosphorylation. In addition, other substrates of the CAK complex have been identified when CAK is assembled with the TFIIH core proteins, thereby regulating transcription and nucleotide excision repair. Little is known about the regulation of the CAK complex through cyclin H. In this study we further analyzed cyclin H regulation and identified two basic clusters in the C terminus of the protein as putative nuclear localization sequences (NLSs). Fusion constructs of full-length and truncated cyclin H sequences demonstrated the functionality of the NLSs. A peptide-binding assay revealed that at least one NLS interacts with the nuclear import receptors importin alpha/beta. Phosphorylation in the vicinity of the NLSs by cyclin C/cdk8 or protein kinase CK2, however, does not influence the nuclear translocation of cyclin H.

Amino Acid Sequence↗
PubMed2005

Molecular cloning and genetic mapping of perennial ryegrass casein protein kinase 2 alpha-subunit genes.

The alpha-subunit of the casein protein kinase CK2 has been implicated in both light-regulated and circadian rhythm-controlled plant gene expression, including control of the flowering time. Two putative CK2alpha genes of perennial ryegrass (Lolium perenne L.) have been obtained from a cDNA library constructed with mRNA isolated from cold-acclimated crown tissue. The genomic organisation of the two genes was determined by Southern hybridisation analysis. Primer designs to the Lpck2a-1 and Lpck2a-2 cDNA sequences permitted the amplification of genomic products containing large intron sequences. Amplicon sequence analysis detected single nucleotide polymorphisms (SNPs) within the p150/112 reference mapping population. Validated SNPs, within diagnostic restriction enzyme sites, were used to design cleaved amplified polymorphic sequence (CAPS) assays. The Lpck2a-1 CAPS marker was assigned to perennial ryegrass linkage group (LG) 4 and the Lpck2a-2 CAPS marker was assigned to LG2. The location of the Lpck2a-1 gene locus supports the previous conclusion of conserved synteny between perennial ryegrass LG4, the Triticeae homoeologous group 5L chromosomes and the corresponding segment of rice chromosome 3. Allelic variation at the Lpck2a-1 and Lpck2a-2 gene loci was correlated with phenotypic variation for heading date and winter survival, respectively. SNP polymorphism may be used for the further study of the role of CK2alpha genes in the initiation of reproductive development and winter hardiness in grasses.

Amino Acid Sequence↗