Disease relevance of MTA2

• Here we report evidence that although both human MTA1 and MTA2 repress transcription specifically, are located in the nucleus, and contain associated histone deacetylase activity, they exist in two biochemically distinct protein complexes and may perform different functions pertaining to tumor metastasis [1].
• We demonstrate that MTA2 expression is correlated with ERalpha protein expression in invasive breast tumors [2].
• The use of intrauterine devices (IUD) in 690 patients admitted to hospital for pelvic inflammatory disease (PID or acute salpingitis) was compared with the use in a sexually active age-matched control group [3].
• After exposure to a child with a respiratory infection on PID 30, V.L.C. (the patient) developed a fulminant pump-pocket infection [4].
• The presence of antibodies to pili of Neisseria gonorrhoeae and Chlamydia trachomatis serovar L2 were assessed in women consecutively hospitalized in Zimbabwe with pelvic inflammatory disease (PID; n = 66), infertility (n = 227), and ectopic pregnancy (n = 60) [5].

Psychiatry related information on MTA2

• Even if they survive, as many as 15% to 20% of these women experience long-term sequelae of PID, such as ectopic pregnancy, tubo-ovarian abscess, infertility, dyspareunia, and chronic pelvic pain [6].
• In congenic mice infected with CJD, PID appears to be located on chromosome 17 in the major histocompatibility complex (H-2) in the D-subregion [7].

High impact information on MTA2

• PID expression strongly represses p53-dependent transcriptional activation, and, notably, it modulates p53-mediated cell growth arrest and apoptosis [8].
• MTA2 modulates the enzymatic activity of the histone deacetylase core complex [9].
• MBD3 mediates the association of MTA2 with the core histone deacetylase complex [9].
• We suggest that MTA1 associates with a different set of transcription factors from MTA2 and that this property may contribute to the metastatic potential of cells overexpressing MTA1 [1].
• The superfamily is named PID (proliferation, ion, and death) because prohibitins are involved in proliferation and cell cycle control, stomatins are involved in ion channel regulation, and the plant defense-related genes are involved in cell death [10].

Chemical compound and disease context of MTA2

• A five-fold increased risk of hospitalized pelvic infection among Dalkon Shield users found in the Women's Health Study resulted not from ascertainment bias, but was related to the fact that Dalkon Shield users had more severe hospitalized PID than did other hospitalized women with PID and IUD use [11].
• The second model (PID) described the response in terms of a proportional component without delay, an integral component that adjusted basal delivery in proportion to hyper/hypoglycemia, and a derivative component that responded to the rate of glucose change [12].
• The incidence of ectopic pregnancy has been steadily growing during the past decade; this fact can only partially be related to known factors (PID, use of IUDs, minipill, inductors of ovulation, sterilization reversal) [13].

Biological context of MTA2

• MTA2, which is homologous to MTA1, is a component of the NuRD ATP-dependent chromatin remodeling and histone deacetylase complex [1].
• Structural analysis of the MTA1-L1 gene revealed 18 exons spanning 8.1 kb of genomic DNA [14].
• This cDNA, named MTA1-L1 (MTA1 like 1), consists of 2736 nucleotides with an open reading frame encoding 668 amino acids [14].
• The region of Fe65 containing the PID/PTB domains was used as a bait to screen a human brain cDNA library in yeast by the two-hybrid system [15].
• Antibodies to C. trachomatis were associated with a history of PID, being single, a positive Treponema pallidum hemagglutination assay, and chlamydial antibody [5].

Anatomical context of MTA2

• The organism has also been isolated in the endometrium and fallopian tubes of women who have PID.The evidence is therefore accumulating that M genitalium is a cause of PID, and the assessment of reliable tests to further investigate the importance of this organism and its relevance in designing future treatment strategies is urgently needed [16].
• Presuming that an increase in PID had a negative effect on metabolism of the intervertebral disc, our results may help to explain why progressive degeneration occurs in these segments [17].
• We examined microbial isolates from the endocervical and peritoneal cavity of 30 women hospitalized with acute PID [18].
• The GC positivity rates which were significantly higher than expected were found in patients with abnormal uterine bleeding, urinary tract symptoms, and cervicitis, as well as acute PID [19].
• The GPC outperformed the MPC and PID controllers when applied to the cultivation of hybridoma cells [20].

Associations of MTA2 with chemical compounds

• MTA1, MTA2, and MTA3 are components of the nucleosome remodeling and deacetylation complex, which is associated with adenosine triphosphate-dependent chromatin remodeling and transcriptional regulation [21].
• Except for a transient increased risk after IUD insertions, increased risk is seen mainly in case-control studies after 1973, the time of a major PID epidemic and adverse publicity related to the Dalkon Shield [22].
• Oxycodone 5 mg/ibuprofen 400 mg was significantly more effective compared with the other treatments on all secondary end points (P < 0.001, all variables except peak PID vs oxycodone 5 mg/acetaminophen 325 mg [P = 0.006]), with the exception of the time to onset of analgesia [23].
• Whenever possible, women with PID should be hospitalized for parenteral therapy [24].
• We conclude that it is appropriate in women with this stage of PID to treat initially with clindamycin and an aminoglycoside [25].

Physical interactions of MTA2

• Specifically, both MTA1 and MTA2 complexes exert histone deacetylase activity [1].

Other interactions of MTA2

• MTA2 expression seems to be unrelated to ER status [26].

Analytical, diagnostic and therapeutic context of MTA2

• A single 3.0-kb transcript of MTA1-L1 was expressed ubiquitously on Northern blots [14].
• We assigned the MTA1-L1 locus to chromosomal band 11q12-13.1 by fluorescence in situ hybridization [14].
• Molecular cloning, mapping, and characterization of a novel human gene, MTA1-L1, showing homology to a metastasis-associated gene, MTA1 [14].
• Of independent importance for infertility, ectopic pregnancy, and time between PID and first intrauterine pregnancy were number of infections, severity of the infections, contraception at the index laparoscopy, age, and delayed treatment [27].
• PID was thought to be a major contributor to the higher costs associated with management of patients with induced abortions [28].

References