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Expression of RING Finger Protein 38 in Serotonergic Neurons in the Brain of Nile Tilapia, Oreochromis niloticus

Cham KL, Soga T, Parhar IS

Front Neuroanat, 2018;12:109.
PMID: 30574074 DOI: 10.3389/fnana.2018.00109

Serotonin (5-hydroxytryptamine, 5-HT) is one of the major neurotransmitters, modulating diverse behaviours and physiological functions. Really interesting new gene (RING) finger protein 38 (RNF38) is an E3 ubiquitin ligase whose function remains unclear. A recent study has shown a possible regulatory relationship between RNF38 and the 5-HT system. Therefore, to gain insight into the role of RNF38 in the central 5-HT system, we identified the neuroanatomical location of 5-HT positive cells and investigated the relationship between RNF38 and the 5-HT system in the brain of the Nile tilapia, Oreochromis niloticus. Immunocytochemistry revealed three neuronal populations of 5-HT in the brain of tilapia; the paraventricular organ (PVO), the dorsal and ventral periventricular pretectal nuclei (PPd and PPv), and, the superior and inferior raphe (SR and IR). The 5-HT neuronal number was highest in the raphe (90.4 in SR, 284.6 in IR), followed by the pretectal area (22.3 in PPd, 209.8 in PPv). Double-label immunocytochemistry showed that the majority of 5-HT neurons express RNF38 nuclear proteins (66.5% in PPd; 77.9% in PPv; 35.7% in SR; 49.1% in IR). These findings suggest that RNF38 could be involved in E3 ubiquitination in the central 5-HT system.

Matched MeSH terms: Nuclear Proteins
Fulltext The rare primary Low Grade Papillary Adenocarcinoma of Nasopharynx: a diagnostic challenge and management

Noor Dina, H., Gendeh, B.S.

Medicine & Health, 2015;10(2):137-140.
MyJurnal

Low Grade Papillary Nasopharyngeal Adenocarcinoma (LGPAC) is a very rare tumour of mucosal origin compared to a higher incidence of well differentiated keratinized/non-keratinized nasopharyngeal carcinoma. It is an epithelial tumour with glandular differentiation. Its papillary figure seen histologically, is also seen in metastatic papillary thyroid carcinoma. This has caused a significant challenge to the Pathologist to differentiate primary papillary nasopharyngeal adenocarcinoma and metastatic tumour. Thyroid Transcription Factor-1 (TTF-1) is also expressed in subsets of papillary nasopharyngeal adenocarcinoma, which is valuable as a diagnostic tool. LGPAC is a benign-like malignant neoplasm. An early diagnosis with a complete tumour removal via conventional excision or endoscopic approach has offered a good prognosis with low risk of recurrence.

Matched MeSH terms: Nuclear Proteins
Fulltext JMJD8 is a positive regulator of TNF-induced NF-κB signaling

Yeo KS, Tan MC, Wong WY, Loh SW, Lam YL, Tan CL, et al.

Sci Rep, 2016 Sep 27;6:34125.
PMID: 27671354 DOI: 10.1038/srep34125

TNF-induced signaling mediates pleiotropic biological consequences including inflammation, immunity, cell proliferation and apoptosis. Misregulation of TNF signaling has been attributed as a major cause of chronic inflammatory diseases and cancer. Jumonji domain-containing protein 8 (JMJD8) belongs to the JmjC family. However, only part of the family members has been described as hydroxylase enzymes that function as histone demethylases. Here, we report that JMJD8 positively regulates TNF-induced NF-κB signaling. Silencing the expression of JMJD8 using RNA interference (RNAi) greatly suppresses TNF-induced expression of several NF-κB-dependent genes. Furthermore, knockdown of JMJD8 expression reduces RIP ubiquitination, IKK kinase activity, delays IκBα degradation and subsequently blocks nuclear translocation of p65. In addition, JMJD8 deficiency enhances TNF-induced apoptosis. Taken together, these findings indicate that JMJD8 functions as a positive regulator of TNF-induced NF-κB signaling.

Matched MeSH terms: Nuclear Proteins
Fulltext HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction

Paudel YN, Shaikh MF, Chakraborti A, Kumari Y, Aledo-Serrano Á, Aleksovska K, et al.

Front Neurosci, 2018;12:628.
PMID: 30271319 DOI: 10.3389/fnins.2018.00628

High mobility group box protein 1 (HMGB1) is a ubiquitous nuclear protein released by glia and neurons upon inflammasome activation and activates receptor for advanced glycation end products (RAGE) and toll-like receptor (TLR) 4 on the target cells. HMGB1/TLR4 axis is a key initiator of neuroinflammation. In recent days, more attention has been paid to HMGB1 due to its contribution in traumatic brain injury (TBI), neuroinflammatory conditions, epileptogenesis, and cognitive impairments and has emerged as a novel target for those conditions. Nevertheless, HMGB1 has not been portrayed as a common prognostic biomarker for these HMGB1 mediated pathologies. The current review discusses the contribution of HMGB1/TLR4/RAGE signaling in several brain injury, neuroinflammation mediated disorders, epileptogenesis and cognitive dysfunctions and in the light of available evidence, argued the possibilities of HMGB1 as a common viable biomarker of the above mentioned neurological dysfunctions. Furthermore, the review also addresses the result of preclinical studies focused on HMGB1 targeted therapy by the HMGB1 antagonist in several ranges of HMGB1 mediated conditions and noted an encouraging result. These findings suggest HMGB1 as a potential candidate to be a common biomarker of TBI, neuroinflammation, epileptogenesis, and cognitive dysfunctions which can be used for early prediction and progression of those neurological diseases. Future study should explore toward the translational implication of HMGB1 which can open the windows of opportunities for the development of innovative therapeutics that could prevent several associated HMGB1 mediated pathologies discussed herein.

Matched MeSH terms: Nuclear Proteins
Fulltext WDR5, ASH2L, and RBBP5 control the efficiency of FOS transcript processing

Teoh PL, Sharrocks AD

Cell Mol Biol Lett, 2014 Jun;19(2):215-32.
PMID: 24715476 DOI: 10.2478/s11658-014-0190-8

H3K4 trimethylation is strongly associated with active transcription. The deposition of this mark is catalyzed by SET-domain methyltransferases, which consist of a subcomplex containing WDR5, ASH2L, and RBBP5 (the WAR subcomplex); a catalytic SET-domain protein; and additional complexspecific subunits. The ERK MAPK pathway also plays an important role in gene regulation via phosphorylation of transcription factors, co-regulators, or histone modifier complexes. However, the potential interactions between these two pathways remain largely unexplored. We investigated their potential interplay in terms of the regulation of the immediate early gene (IEG) regulatory network. We found that depletion of components of the WAR subcomplex led to increased levels of unspliced transcripts of IEGs that did not necessarily reflect changes in their mature transcripts. This occurs in a manner independent from changes in the H3K4me3 levels at the promoter region. We focused on FOS and found that the depletion of WAR subcomplex components affected the efficiency of FOS transcript processing. Our findings show a new aspect of WAR subcomplex function in coordinating active transcription with efficient pre-mRNA processing.

Matched MeSH terms: Nuclear Proteins/antagonists & inhibitors; Nuclear Proteins/genetics; Nuclear Proteins/metabolism*
Fulltext Identification of a BET family bromodomain/casein kinase II/TAF-containing complex as a regulator of mitotic condensin function

Kim HS, Mukhopadhyay R, Rothbart SB, Silva AC, Vanoosthuyse V, Radovani E, et al.

Cell Rep, 2014 Mar 13;6(5):892-905.
PMID: 24565511 DOI: 10.1016/j.celrep.2014.01.029

Condensin is a central regulator of mitotic genome structure with mutants showing poorly condensed chromosomes and profound segregation defects. Here, we identify NCT, a complex comprising the Nrc1 BET-family tandem bromodomain protein (SPAC631.02), casein kinase II (CKII), and several TAFs, as a regulator of condensin function. We show that NCT and condensin bind similar genomic regions but only briefly colocalize during the periods of chromosome condensation and decondensation. This pattern of NCT binding at the core centromere, the region of maximal condensin enrichment, tracks the abundance of acetylated histone H4, as regulated by the Hat1-Mis16 acetyltransferase complex and recognized by the first Nrc1 bromodomain. Strikingly, mutants in NCT or Hat1-Mis16 restore the formation of segregation-competent chromosomes in cells containing defective condensin. These results are consistent with a model where NCT targets CKII to chromatin in a cell-cycle-directed manner in order to modulate the activity of condensin during chromosome condensation and decondensation.

Matched MeSH terms: Nuclear Proteins/metabolism*
Fulltext Prevalence of PALB2 mutations in breast cancer patients in multi-ethnic Asian population in Malaysia and Singapore

Phuah SY, Lee SY, Kang P, Kang IN, Yoon SY, Thong MK, et al.

PLoS One, 2013;8(8):e73638.
PMID: 23977390 DOI: 10.1371/journal.pone.0073638

The partner and localizer of breast cancer 2 (PALB2) is responsible for facilitating BRCA2-mediated DNA repair by serving as a bridging molecule, acting as the physical and functional link between the breast cancer 1 (BRCA1) and breast cancer 2 (BRCA2) proteins. Truncating mutations in the PALB2 gene are rare but are thought to be associated with increased risks of developing breast cancer in various populations.

Matched MeSH terms: Nuclear Proteins/genetics*
Contribution of the MLH1 -93G>a promoter polymorphism in modulating susceptibility risk in Malaysian colorectal cancer patients

Nizam ZM, Abdul Aziz AA, Kaur G, Abu Hassan MR, Mohd Sidek AS, Yeh LY, et al.

Asian Pac J Cancer Prev, 2013;14(2):619-24.
PMID: 23621208

BACKGROUND: Colorectal cancer (CRC) exists in a more common sporadic form and less common hereditary forms, associated with the Lynch syndrome, familial adenomatous polyposis (FAP) and other rare syndromes. Sporadic CRC is believed to arise as a result of close interaction between environmental factors, including dietary and lifestyle habits, and genetic predisposition factors. In contrast, hereditary forms such as those related to the Lynch syndrome result from inheritance of germline mutations of mismatch repair (MMR) genes. However, in certain cases, the influence of low penetrance alleles in familial colorectal cancer susceptibility is also undeniable.
AIM: To investigate the genotype frequencies of MLH1 promoter polymorphism -93G>A and to determine whether it could play any role in modulating familial and sporadic CRC susceptibility risk.
METHODS: A case-control study comprising of 104 histopathologically confirmed CRC patients as cases (52 sporadic CRC and 52 Lynch syndrome patients) and 104 normal healthy individuals as controls was undertaken. DNA was extracted from peripheral blood and the polymorphism was genotyped employing PCR-RFLP methods. The genotypes were categorized into homozygous wild type, heterozygous and homozygous variants. The risk association between these polymorphisms and CRC susceptibility risk was calculated using binary logistic regression analysis and deriving odds ratios (ORs).
RESULTS: When risk association was investigated for all CRC patients as a single group, the heterozygous (G/A) genotype showed a significantly higher risk for CRC susceptibility with an OR of 2.273, (95%CI: 1.133-4.558 and p-value=0.021). When analyzed specifically for the 2 types of CRC, the heterozygous (G/A) genotype showed significantly higher risk for sporadic CRC susceptibility with and OR of 3.714, (95%CI: 1.416-9.740 and p-value=0.008). Despite high OR value was observed for Lynch syndrome (OR: 1.600, 95%CI: 0.715-3.581), the risk was not statistically significant (P=0.253).
CONCLUSION: Our results suggest an influence of MLH1 promoter polymorphism -93G>A in modulating susceptibility risk in Malaysian CRC patients, especially those with sporadic disease.

Matched MeSH terms: Nuclear Proteins/genetics*
RET and p53 expression in thyroid follicular adenoma: a study of 52 cases with 14 years follow-up

Othman NH, Omar E, Mahmood MH, Madhavan M

Malays J Pathol, 2005 Dec;27(2):91-8.
PMID: 17191391

Most previous studies on RET and p53 proteins have focused on thyroid papillary carcinoma. We investigated the role of RET and p53 protein expressions using immunohistochemistry on 52 cases of thyroid follicular adenomas and studied the follow-up records of these patients. The range of follow-up period was 3 to 14 years. The patients were between 15 and 71 years of age with a median age of 34.5 years. There were 46 females and 6 males. Except for 3 cases, all patients were Malays. The minimum volume of the tumour was 1000 mm3 and the maximum was 512,000 mm3 with a median of 270,000 mm3. Eleven (21.2%) cases showed RET expression. RET expression was not statistically significant when cross-tabulated against sex (p = 0.322), ethnicity (p = 0.518), age (p = 0.466) and symptom duration (p = 0.144). Six (11.5%) of 52 cases showed p53 immunopositivity. p53 expressions were also not significantly correlated to the clinical parameters above. There was no correlation between RET and p53 protein expressions. The only statistically significant finding was the association of tumour volume with duration of symptoms (p = 0.05). All patients are alive at the time of writing. 3 had recurrent goitre, 2 of these were diagnosed as colloid goitre while the third was a follicular lesion. One patient suffered from depression requiring anti-depressant treatment. In conclusion, unlike papillary carcinoma in which the roles of ret and p53 oncogenes are known, their roles in influencing the behaviour of follicular adenoma has not been ascertained.

Matched MeSH terms: Nuclear Proteins/biosynthesis*
Fulltext Co-Expression of TWIST1 and ZEB2 in Oral Squamous Cell Carcinoma Is Associated with Poor Survival

Kong YH, Syed Zanaruddin SN, Lau SH, Ramanathan A, Kallarakkal TG, Vincent-Chong VK, et al.

PLoS One, 2015;10(7):e0134045.
PMID: 26214683 DOI: 10.1371/journal.pone.0134045

Oral squamous cell carcinoma (OSCC) is an aggressive disease accounting for more than 260,000 cancer cases diagnosed and 128,000 deaths worldwide. A large majority of cancer deaths result from cancers that have metastasized beyond the primary tumor. The relationship between genetic changes and clinical outcome can reflect the biological events that promote cancer's aggressive behavior, and these can serve as molecular markers for improved patient management and survival. To this end, epithelial-mesenchymal transition (EMT) is a major process that promotes tumor invasion and metastasis, making EMT-related proteins attractive diagnostic biomarkers and therapeutic targets. In this study, we used immunohistochemistry to study the expression of a panel of transcription factors (TWIST1, SNAI1/2, ZEB1 and ZEB2) and other genes intimately related to EMT (CDH1 and LAMC2) at the invasive tumor front of OSCC tissues. The association between the expression of these proteins and clinico-pathological parameters were examined with Pearson Chi-square and correlation with survival was analyzed using Kaplan Meier analysis. Our results demonstrate that there was a significant differential expression of CDH1, LAMC2, SNAI1/2 and TWIST1 between OSCC and normal oral mucosa (NOM). Specifically, CDH1 loss was significantly associated with Broder's grading, while diffused LAMC2 was similarly associated with non-cohesive pattern of invasion. Notably, co-expression of TWIST1 and ZEB2 in OSCC was significantly associated with poorer overall survival, particularly in patients without detectable lymph node metastasis. This study demonstrates that EMT-related proteins are differentially expressed in OSCC and that the co-expression of TWIST1 and ZEB2 could be of clinical value in identifying patients with poor survival for appropriate patient management.

Matched MeSH terms: Nuclear Proteins/biosynthesis*
Fulltext Identification of FLT3 and NPM1 Mutations in Patients with Acute Myeloid Leukaemia

Mat Yusoff Y, Abu Seman Z, Othman N, Kamaluddin NR, Esa E, Zulkiply NA, et al.

Asian Pac J Cancer Prev, 2019 06 01;20(6):1749-1755.
PMID: 31244296 DOI: 10.31557/APJCP.2019.20.6.1749

Objective: The most frequent acquired molecular abnormalities and important prognostic indicators in patients
with Acute Myeloid Leukaemia (AML) are fms-like tyrosine kinase-3 gene (FLT3) and nucleophosmin-1 (NPM1)
mutations. Our study aims to develop a cost effective and comprehensive in-house conventional PCR method for
detection of FLT3-ITD, FLT3-D835 and NPM1 mutations and to evaluate the frequency of these mutations in patients
with cytogenetically normal (CN) AML in our population. Methods: A total of 199 samples from AML patients (95
women, 104 men) were included in the study. Mutation analyses were performed using polymerase chain reaction
(PCR) and gene sequencing. Result: Sixty-eight patients were positive for the mutations. FLT3-ITD mutations were
detected in 32 patients (16.1%), followed by FLT3-D835 in 5 (2.5%) and NPM1 in 54 (27.1%). Double mutations of
NPM1 and FLT3-ITD were detected in 23 cases (11.6%). Assays validation were performed using Sanger sequencing
and showed 100% concordance with in house method. Conclusion: The optimized in-house PCR assays for the
detection of FLT3-ITD, FLT3-D835 and NPM1 mutations in AML patients were robust, less labour intensive and cost
effective. These assays can be used as diagnostic tools for mutation detection in AML patients since identification of
these mutations are important for prognostication and optimization of patient care.

Matched MeSH terms: Nuclear Proteins/genetics*
Role of Epithelial-to-Mesenchymal Transition Markers in Different Stages of Endometriosis: Expression of the Snail, Slug, ZEB1, and Twist Genes

Kazmi I, Alharbi KS, Al-Abbasi FA, Almalki WH, G SK, Yasmeen A, et al.

Crit Rev Eukaryot Gene Expr, 2021;31(2):89-95.
PMID: 34347983 DOI: 10.1615/CritRevEukaryotGeneExpr.2021037996

Among various epithelial-to-mesenchymal transition (EMT)-related transcription factors (TFs), altered expression levels of Snail-1, Snail-2/Slug, Twist, and ZEB1 have shown a significant association in different cancers having a higher risk of metastasis. However, their role in the circulation of endometriosis patients is not well understood. Hence, the present study was designed to evaluate the crucial role of these TFs in defining the molecular pathogenesis for endometriosis progression and differentiation from control subjects. The qualitative and quantitative expression analysis of Snail-1, Snail-2/Slug, Twist, and ZEB1 were analyzed in peripheral blood samples of 75 different stages of endometriosis patients and compared with 50 control subjects. Total RNA was extracted and converted into complementary DNA (cDNA) for relative quantification of each gene transcript using SYBRGreen-based reverse transcriptase quantitative polymerase chain reaction (RT-qPCR). The Livak method of relative quantification was used for calculating the fold change in each TF compared with endogenous control. All four selected TFs showed significantly upregulated expression levels in endometriosis patients compared with control subjects. A three-fold increase was observed for Snail-1 (p = 0.0001), and a two-fold increase was observed for Snail-2 (p = 0.01), Twist (p = 0.0002), and ZEB1 (p = 0.001) in stage III and IV compared with stage I and II of endometriosis patients. The present study revealed that EMT-related TFs play a crucial role in the pathogenesis and differentiating different stages of endometriosis patients through expression analysis of specific molecular cascades using non-invasive tools.

Matched MeSH terms: Nuclear Proteins/genetics*
Fulltext rs2735383, located at a microRNA binding site in the 3'UTR of NBS1, is not associated with breast cancer risk

Liu J, Lončar I, Collée JM, Bolla MK, Dennis J, Michailidou K, et al.

Sci Rep, 2016 Nov 15;6:36874.
PMID: 27845421 DOI: 10.1038/srep36874

NBS1, also known as NBN, plays an important role in maintaining genomic stability. Interestingly, rs2735383 G > C, located in a microRNA binding site in the 3'-untranslated region (UTR) of NBS1, was shown to be associated with increased susceptibility to lung and colorectal cancer. However, the relation between rs2735383 and susceptibility to breast cancer is not yet clear. Therefore, we genotyped rs2735383 in 1,170 familial non-BRCA1/2 breast cancer cases and 1,077 controls using PCR-based restriction fragment length polymorphism (RFLP-PCR) analysis, but found no association between rs2735383CC and breast cancer risk (OR = 1.214, 95% CI = 0.936-1.574, P = 0.144). Because we could not exclude a small effect size due to a limited sample size, we further analyzed imputed rs2735383 genotypes (r2 > 0.999) of 47,640 breast cancer cases and 46,656 controls from the Breast Cancer Association Consortium (BCAC). However, rs2735383CC was not associated with overall breast cancer risk in European (OR = 1.014, 95% CI = 0.969-1.060, P = 0.556) nor in Asian women (OR = 0.998, 95% CI = 0.905-1.100, P = 0.961). Subgroup analyses by age, age at menarche, age at menopause, menopausal status, number of pregnancies, breast feeding, family history and receptor status also did not reveal a significant association. This study therefore does not support the involvement of the genotype at NBS1 rs2735383 in breast cancer susceptibility.

Matched MeSH terms: Nuclear Proteins/genetics*
Fulltext Evolutionary and functional analysis of RBMY1 gene copy number variation on the human Y chromosome

Shi W, Louzada S, Grigorova M, Massaia A, Arciero E, Kibena L, et al.

Hum Mol Genet, 2019 Aug 15;28(16):2785-2798.
PMID: 31108506 DOI: 10.1093/hmg/ddz101

Human RBMY1 genes are located in four variable-sized clusters on the Y chromosome, expressed in male germ cells and possibly associated with sperm motility. We have re-investigated the mutational background and evolutionary history of the RBMY1 copy number distribution in worldwide samples and its relevance to sperm parameters in an Estonian cohort of idiopathic male factor infertility subjects. We estimated approximate RBMY1 copy numbers in 1218 1000 Genomes Project phase 3 males from sequencing read-depth, then chose 14 for valid ation by multicolour fibre-FISH. These fibre-FISH samples provided accurate calibration standards for the entire panel and led to detailed insights into population variation and mutational mechanisms. RBMY1 copy number worldwide ranged from 3 to 13 with a mode of 8. The two larger proximal clusters were the most variable, and additional duplications, deletions and inversions were detected. Placing the copy number estimates onto the published Y-SNP-based phylogeny of the same samples suggested a minimum of 562 mutational changes, translating to a mutation rate of 2.20 × 10-3 (95% CI 1.94 × 10-3 to 2.48 × 10-3) per father-to-son Y-transmission, higher than many short tandem repeat (Y-STRs), and showed no evidence for selection for increased or decreased copy number, but possible copy number stabilizing selection. An analysis of RBMY1 copy numbers among 376 infertility subjects failed to replicate a previously reported association with sperm motility and showed no significant effect on sperm count and concentration, serum follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone levels or testicular and semen volume. These results provide the first in-depth insights into the structural rearrangements underlying RBMY1 copy number variation across diverse human lineages.

Matched MeSH terms: Nuclear Proteins/genetics*
Methicillin-susceptible and -resistant Staphylococcus aureus with high-level antiseptic and low-level mupirocin resistance in Malaysia

Ghasemzadeh-Moghaddam H, van Belkum A, Hamat RA, van Wamel W, Neela V

Microb Drug Resist, 2014 Oct;20(5):472-7.
PMID: 24841796 DOI: 10.1089/mdr.2013.0222

The prevalence and spread of mupirocin and antiseptic resistance among colonizing and infectious Staphylococcus aureus were determined. S. aureus isolated from anterior nares and infection sites of patients hospitalized in the largest tertiary care referral hospital in Malaysia was investigated for mupirocin and antiseptic susceptibility testing, and for PCR detection of mupA, qacA/B, and smr genes. Twelve isolates showed resistance to mupirocin by disk diffusion, of which 10 (3.8%) harbored the mupA gene. Minimum inhibitory concentrations (MICs) ranged from 64 to 768 μg/ml for mupA positive and below 46 μg/ml for negative isolates. The mupA was more common among ST239 isolates (70%). The qacA/B was carried in 67 out of 95 methicillin-resistant Staphylococcus aureus (MRSA) (70.5%) and 3 out of 164 methicillin-susceptible Staphylococcus aureus (MSSA) (1.8%), while smr was carried in 6 out of 95 MRSA (6.3%) strains. MICs ranged from 3.9 to 15.6 μg/ml for benzethonium chloride (BTC) and benzalkonium chloride (BKC), and from 10.3 to 20.7 μg/ml for chlorhexidine digluconate (CHG). Isolates with qacA/B and smr or qacA/B alone showed higher MIC (20.7 μg/ml for CHG and 15.6 μg/ml for BTC and BKC) than the isolates that lacked antiseptic resistance genes (10.3 μg/ml for CHG and 3.9 μg/ml for BTC and BKC). In 16 cases, ST239 was isolated from the infection site and the nares simultaneously, and shared identical resistance patterns (qacAB or qacAB+smr), suggesting possible endogenous infection. Spread of low-level mupirocin resistance expressing ST239 MRSA and high-level resistance expressing emerging ST1, co-existing with antiseptic-resistant genes showing elevated MICs, should be monitored for effective infection control.

Matched MeSH terms: Nuclear Proteins/genetics; Nuclear Proteins/metabolism
Human nasal turbinates as a viable source of respiratory epithelial cells using co-culture system versus dispase-dissociation technique

Noruddin NA, Saim AB, Chua KH, Idrus R

Laryngoscope, 2007 Dec;117(12):2139-45.
PMID: 17891046

OBJECTIVE: To compare a co-culture system with a conventional dispase-dissociation method for obtaining functional human respiratory epithelial cells from the nasal turbinates for tissue engineering application.
METHODS: Human respiratory epithelial cells were serially passaged using a co-culture system and a conventional dispase-dissociation technique. The growth kinetics and gene expression levels of the cultured respiratory epithelial cells were compared. Four genes were investigated, namely cytokeratin-18, a marker for ciliated and secretory epithelial cells; cytokeratin-14, a marker for basal epithelial cells; MKI67, a proliferation marker; and MUC5B, a marker for mucin secretion. Immunocytochemical analysis was performed using monoclonal antibodies against the high molecular-weight cytokeratin 34 beta E12, cytokeratin 18, and MUC5A to investigate the protein expression from cultured respiratory epithelial cells.
RESULTS: Respiratory epithelial cells cultured using both methods maintained polygonal morphology throughout the passages. At passage 1, co-cultured respiratory epithelial showed a 2.6-times higher growth rate compared to conventional dispase dissociation technique, and 7.8 times higher at passage 2. Better basal gene expression was observed by co-cultured respiratory epithelial cells compared to dispase dissociated cells. Immunocytochemical analyses were positive for the respiratory epithelial cells cultured using both techniques.
CONCLUSION: Co-culture system produced superior quality of cultured human respiratory epithelial cells from the nasal turbinates as compared to dispase dissociation technique.

Matched MeSH terms: Nuclear Proteins/biosynthesis; Nuclear Proteins/genetics
Fulltext Sumoylation controls the timing of Tup1-mediated transcriptional deactivation

Ng CH, Akhter A, Yurko N, Burgener JM, Rosonina E, Manley JL

Nat Commun, 2015 Mar 13;6:6610.
PMID: 25766875 DOI: 10.1038/ncomms7610

The small ubiquitin-like modifier (SUMO) is implicated in various cellular activities, including transcriptional regulation. We previously showed that the yeast activator Gcn4 becomes sumoylated during activation, facilitating its eventual promoter eviction and transcriptional shut off. Here we show that the corepressor Tup1 is sumoylated, at two specific lysines, under various stress conditions. Mutation of these sites has no effect on Tup1 recruitment or RNAP II promoter occupancy immediately following induction. However, Tup1 levels subsequently decrease, while RNAP II and transcription increase in Tup1 mutant cells. Consistent with this, a Tup1 mutant displaying increased sumoylation led to reduced transcription. We also show that coordinated sumoylation of Gcn4 and Tup1 enhances Gcn4 promoter eviction and that multiple Tup1-interacting proteins become sumoylated after stress. Together, our studies provide evidence that coordinated sumoylation of Gcn4, Tup1 and likely other factors dampens activated transcription by stabilizing Tup1 binding and stimulating Gcn4 and RNAP II removal.

Matched MeSH terms: Nuclear Proteins/metabolism*
Fulltext Mutant p53 mediates survival of breast cancer cells

Lim LY, Vidnovic N, Ellisen LW, Leong CO

Br. J. Cancer, 2009 Nov 3;101(9):1606-12.
PMID: 19773755 DOI: 10.1038/sj.bjc.6605335

p53 is the most commonly mutated tumour-suppressor gene in human cancers. Unlike other tumour-suppressor genes, most p53 cancer mutations are missense mutations within the core domain, leading to the expression of a full-length mutant p53 protein. Accumulating evidence has indicated that p53 cancer mutants not only lose tumour suppression activity but also gain new oncogenic activities to promote tumourigenesis.

Matched MeSH terms: Nuclear Proteins/physiology
Minichromosome maintenance protein 2 is a reliable proliferative marker in breast carcinoma

Reena RM, Mastura M, Siti-Aishah MA, Munirah MA, Norlia A, Naqiyah I, et al.

Ann Diagn Pathol, 2008 Oct;12(5):340-3.
PMID: 18774496 DOI: 10.1016/j.anndiagpath.2008.04.001

This is a study aimed to examine the distribution pattern of a specific minichromosome maintenance protein 2 (MCM2) in benign and malignant breast tissue. We also aim to correlate the frequency of expression of MCM2 with the degree of tumor differentiation. We used immunohistochemistry to examine the distribution and expression pattern of MCM2 on formalin-fixed paraffin-embedded tissue sections of benign (n = 30) and malignant breast tissue (n = 70) (IDC 56, DCIS 4, ILC 2, nonductal 4, mixed type 4). We quantified MCM2 expression by calculating a labeling index, which represents the percentage of epithelial nuclei that stained positively. Immunoreactivity was heterogenous in all the 70 malignant cases examined. Epithelial cells in cycle are most frequent at the tumor periphery. Labeling index of MCM2 was greatest in grade 3 (poorly differentiated) and lowest in grade 1 tumors (well differentiated). Minichromosome maintenance protein 2 expression in breast cancer showed a positive association with histologic grade (P < .05). In all the benign breast tissue examined, no proliferating compartments could be characterized. Minichromosome maintenance protein 2 is a useful proliferative marker of breast carcinoma. The frequency of expression of MCM2 showed an inverse correlation with the degree of tumor differentiation.

Matched MeSH terms: Nuclear Proteins/metabolism*
Fulltext ER, p53 and MIB-1 are significantly associated with malignant phyllodes tumor

Munawer NH, Md Zin R, Md Ali SA, Muhammad R, Ali J, Das S

Biomed J, 2012 Nov-Dec;35(6):486-92.
PMID: 23442362 DOI: 10.4103/2319-4170.104414

Fibroadenomas (FA) are common while phyllodes tumors (PT) are rare and both tumors are composed of epithelial and stromal components. We evaluated the expression status of ER, Bc12, p53, and MIB-1 protein in these tumors.

Matched MeSH terms: Nuclear Proteins/metabolism*

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