Disease relevance of LITAF

• PIG7/LITAF gene mutation and overexpression of its gene product in extramammary Paget's disease [1].
• Charcot-Marie-Tooth disease type 1C (CMT1C) is caused by mutations in the small integral membrane protein of the lysosome/late endosome (SIMPLE) [2].
• In patients with CD, a 5-fold increase in LITAF mRNA was measurable in noninflamed colonic tissues compared with controls without inflammatory bowel disease [3].
• Charcot-Marie-Tooth neuropathy type 1C (CMT1C) is an autosomal dominant demyelinating peripheral neuropathy caused by missense mutations in the small integral membrane protein of lysosome/late endosome (SIMPLE) gene [4].
• Charcot-Marie-Tooth neuropathy type 1 (CMT1) is a genetically heterogeneous group of chronic demyelinating polyneuropathies with loci mapping to chromosome 17 (CMT1A), chromosome 1 (CMT1B) and to another unknown autosome (CMT1C) [5].

Psychiatry related information on LITAF

• CONCLUSIONS: Simple, inexpensive interventions can increase physical activity [6].
• CONCLUSION: Simple clinical clues in patients with physical complaints identify a subgroup who may warrant further evaluation for a depressive or anxiety disorder [7].
• MEASUREMENTS: Simple reaction time, prospective self-assessment of performance, and instantaneous fatigue and sleepiness ratings measured at 2-hour intervals [8].
• CONCLUSIONS: Simple smoking cessation advice combined with spirometric testing resulted in good 1 year cessation rates, especially in subjects with airway obstruction [9].
• Risk scores for the Osteoporosis Self-assessment Tool, Osteoporosis Risk Assessment Instrument, and Simple Calculated Osteoporosis Risk Estimation were calculated for each patient [10].

High impact information on LITAF

• Perspectives: epidemiology. Simple rules with complex dynamics [11].
• In addition, the specific role of LITAF in this complex was established with experiments, including RNA interference technology [12].
• Previously, we identified a transcription factor, LPS-induced TNF-alpha factor (LITAF), that regulates TNF-alpha transcription [12].
• The epithelial membrane protein 2 gene (EMP2), which maps to chromosome 16p13.2, was evaluated as a candidate gene for CMT1C [13].
• We report genetic mapping of the disease to chromosome 16p13.1-p12.3, in two families with autosomal dominant CMT type 1C (CMT1C) [13].

Chemical compound and disease context of LITAF

• Clomid for unexplained infertility? Simple lie or complicated truth [14]?
• Based on multiple linear regression, the Simple Endoscopic Score for Crohn's Disease resulted in the sum of the scores for ulcer size, ulcerated surface, affected surface, and luminal narrowing [15].
• All had the following tests: gastric biopsies (2 antral, 1 fundus; H&E and Alcian Yellow stain) examined for gastritis and H pylori; (13)C-UBT; capillary blood for whole blood rapid antibody tests: FlexSure HP, QuickVue, AccuStat, and Stat-Simple Pylori; serum for FlexSure HP; HM-CAP enzyme-linked immunoassay [16].
• The NCTB consists of 7 neurobehavioral tests (Digit Symbol, Digit Span, Benton visual memory test/recognition form, Santa Ana dexterity test, Simple Reaction Time, Pursuit Aiming II, and Profile of Mood States) [17].
• In the 20-29 and the 30-39 age ranges, there was a prevalence of POMS scale scores below 10th percentile rank, in the 50-59 age range, the percentages were high for the Digit Symbol, the mean value of Simple Reaction Time, Serial Digit Learning, and Benton Visual Recognition [18].

Biological context of LITAF

• Clinical, electrophysiological and molecular genetic studies in a family with X-linked dominant Charcot-Marie-Tooth neuropathy presenting a novel mutation in GJB1 Promoter and a rare polymorphism in LITAF/SIMPLE [19].
• Finally, chromosomal localization using fluorescence in situ hybridization revealed that LITAF mapped to chromosome 16p12-16p13 [20].
• 3. Together, these findings suggest that LITAF plays an important role in the activation of the human TNF-alpha gene and proposes a new mechanism to control TNF-alpha gene expression [20].
• This suggests that LITAF mutations can severely affect the CMT phenotype caused by a PMP22 duplication [21].
• Genetic analysis identified the boy as a heterozygote for both a peripheral myelin protein 22 (PMP22) duplication and a mutation in the lipopolysaccharide-induced-tumour-necrosis-factor-alpha-factor (LITAF) gene, whereas each parent only had one mutated CMT gene [21].

Anatomical context of LITAF

• In addition, high level of expression of LITAF mRNA was observed predominantly in the placenta, peripheral blood leukocytes, lymph nodes, and the spleen [20].
• CONCLUSIONS: Mutations in LITAF may account for a significant proportion of CMT1 patients with previously unknown molecular diagnosis and may define a new mechanism of peripheral nerve perturbation leading to demyelinating neuropathy [22].
• The LITAF transcript is expressed in sciatic nerve, but its level of expression is not altered during development or in response to nerve injury [22].
• Western blot analysis suggested that the T115N and W116G mutations do not alter the level of LITAF protein in peripheral blood lymphocytes [22].
• Similarly, in inflamed ileal tissues from patients with CD, LITAF is also localized to lamina propria macrophages [3].

Associations of LITAF with chemical compounds

• 2) The coding region of the transcript differs from LITAF/PIG7 due to an absence of a single guanine residue, resulting in a potential translational frameshift [23].
• A Simple Method for Kinetic Control of DNA-Induced Nanoparticle Assembly [24].
• 24-hour mean pulse. Simple predictor of doxorubicin-induced cardiac damage [25].
• The Mannich Reaction of Malonates with Simple Imines Catalyzed by Bifunctional Cinchona Alkaloids: Enantioselective Synthesis of beta-Amino Acids [26].
• RESULTS: Simple correlation analysis revealed a significant direct correlation in blacks (but not whites) between gonadal androgens and AUC for glucose, insulin, and C-peptide [27].

Physical interactions of LITAF

• In this study, we identify by footprinting a sequence motif, CTCCC (-515 to -511), within the TNF-alpha promoter that binds to hLITAF [28].

Regulatory relationships of LITAF

• List Simple software permitted analysis of each specimen together with its isotype control (IgG1) on the same cytogram so that p53 expression could be determined separately for the diploid and aneuploid populations of aneuploid tumors and for tumor cells of diploid tumors in the various phases of the cell cycle [29].
• CONCLUSIONS: Simple surgical excision of the cyst "membrane" of epileptogenic poroencephalic cysts can represent an excellent means to control epilepsy in affected children [30].

Other interactions of LITAF

• Mutation of a putative protein degradation gene LITAF/SIMPLE in Charcot-Marie-Tooth disease 1C [22].
• Genetic loci for CMT1 map to chromosome 17 (CMT1A), chromosome 1 (CMT1B), and another unknown autosome (CMT1C) [31].
• METHODS: In this report, we identified LITAF in resected ileal and colonic tissues from patients with CD and UC by immunohistochemistry, real-time polymerase chain reaction, and Western blot analysis [3].
• RESULTS: Simple pairwise analyses did not reveal significant association between TNFa polymorphism and RA severity [32].
• We examine three CMT1C-associated SIMPLE mutations and show that they do not affect the interaction with NEDD4 or TSG101, nor do they lead to altered subcellular localization [33].

Analytical, diagnostic and therapeutic context of LITAF

• One sample with amino acid substitution overexpressed PIG7/LITAF mRNA in cDNA array analysis and RT-PCR [1].
• CONCLUSION: Simple markers for the initiation of highly active antiretroviral therapy were identified among HIV-infected Ethiopian patients [34].
• BACKGROUND: Simple criteria are needed to predict which patients with severe ulcerative colitis will respond poorly to intensive medical treatment and require colectomy [35].
• The RPF dependency of GFR in the type 1 diabetics suggests strongly that glomerular filtration equilibrium exists in the glomeruli of the diabetic kidney: Simple notions of local control based on afferent:efferent arteriolar resistance ratios are too simplistic [36].
• RESULTS: Simple linear regression analysis showed a significant correlation between portal perfusion index and BRI1 (p < 0.05, r = -0.43) and BRI2 (p = 0.01, r = -0.53) [37].

References