Disease relevance of Trp53inp1

• Stress-induced failure of cell death programs may lead to an accumulation of damaged cells and therefore enhance the risk for cancer as observed in HT1 and other chronic liver diseases [1].
• A 5' Leader of Rbm3, a Cold Stress-induced mRNA, Mediates Internal Initiation of Translation with Increased Efficiency under Conditions of Mild Hypothermia [2].
• The deduced Sip proteins (denoted SipX, SipY and SipZ) are significantly similar to SipS and SipT, the major SPase I proteins of Bacillus subtilis (38% to 44% peptidic identity) [3].
• Stress-induced hyperthermia in the 5-HT(1A) receptor knockout mouse is normal [4].
• Protection from group B streptococcal infection in neonatal mice by maternal immunization with recombinant Sip protein [5].

Psychiatry related information on Trp53inp1

• Stress-induced analgesia involves activation of the opiate system: thus this type of analgesic mechanism responds to classical conditioning [6].
• Stress-induced impairment of inhibitory avoidance learning in female neuromedin B receptor-deficient mice [7].

High impact information on Trp53inp1

• Stress-induced activation of GADD34 feeds back negatively on this pathway by promoting eIF2alpha dephosphorylation, however, GADD34 mutant cells retain significant eIF2alpha-directed phosphatase activity [8].
• Stress-induced gene expression requires programmed recovery from translational repression [9].
• Stress-induced enhancement of leukocyte trafficking into sites of surgery or immune activation [10].
• Stress-induced cholinergic signaling promotes inflammation-associated thrombopoiesis [11].
• Stress-induced microthrombi formation was pronounced in renal glomeruli and within the vasculature in adipose tissues of aged mice [12].

Chemical compound and disease context of Trp53inp1

• Stress-induced alterations in delayed-type hypersensitivity to SRBC and contact sensitivity to DNFB in mice [13].
• Stress-induced hyperthermia in mice: effects of flesinoxan on heart rate and body temperature [14].
• Stress-induced hyperthermia in the mouse: c-fos expression, corticosterone and temperature changes [15].

Biological context of Trp53inp1

• Stress induced by physical restraint results in depressed macrophage activation [16].
• Bok, Bcl-2-related Ovarian Killer, Is Cell Cycle-regulated and Sensitizes to Stress-induced Apoptosis [17].
• Stress-induced apoptosis associated with null mutation of ADAR1 RNA editing deaminase gene [18].
• Stress-induced alternative splicing of acetylcholinesterase results in enhanced fear memory and long-term potentiation [19].
• A protein of group B streptococci (GBS), named Sip for surface immunogenic protein, which is distinct from previously described surface proteins, was identified after immunological screening of a genomic library [20].

Anatomical context of Trp53inp1

• Among these genes, we report a new serine peptidase highly expressed in cortical epithelial cells that we have named thymus-specific serine peptidase (TSSP), and an acidic protein expressed in thymocytes and of unknown function that we have named thymus-expressed acidic protein (TEAP) [21].
• Stress-induced activation of GATA-4 in cardiac muscle cells [22].
• Examination of GBS cells by immunogold electron microscopy revealed that the Sip-specific antibodies attached preferentially to polar sites and the septal region [23].
• Stress-induced spine loss in the medial amygdala is mediated by tissue-plasminogen activator [24].
• Stress-induced changes attributable to the sympathetic nervous system during experimental influenza viral infection in DBA/2 inbred mouse strain [25].

Associations of Trp53inp1 with chemical compounds

• Chromosomal localization of two mouse genes encoding thymus-specific serine peptidase and thymus-expressed acidic protein [26].
• Contrasting Genome-Wide Distribution of 8-Hydroxyguanine and Acrolein-Modified Adenine during Oxidative Stress-Induced Renal Carcinogenesis [27].
• Stress-induced IL-6 release was absent in W/W(v) mast cell-deficient mice and it was partially inhibited by cromolyn in C57BL and ApoE mice [28].
• Stress-induced analgesia, as determined by increased tail-flick latencies following intraperitoneal injection of acetic acid, was effectively antagonized by naloxone, Ca2+ and Mn2+ [29].
• Stress-induced changes of norepinephrine uptake sites in the locus coeruleus of C57BL/6J and DBA/2J mice: a quantitative autoradiographic study using [3H]-tomoxetine [30].

Other interactions of Trp53inp1

• Stress-induced dura vascular permeability does not develop in mast cell-deficient and neurokinin-1 receptor knockout mice [31].
• Stress-induced interleukin-6 release in mice is mast cell-dependent and more pronounced in Apolipoprotein E knockout mice [28].
• 3. Results: Stress-induced increases in the PNMT mRNA and protein levels observed in WT mice were almost completely absent in CRH KO mouse adrenal medulla, stellate ganglia, and cardiac atria, while ventricular PNMT mRNA elevation was not CRH-dependent [32].
• Stress-induced pressor and corticosterone responses in oxytocin-deficient mice [33].
• Stress-induced JNK activation is independent of Gadd45 induction [34].

Analytical, diagnostic and therapeutic context of Trp53inp1

• Stress-induced analgesia in the mouse: strain comparisons [35].
• The localization and accessibility of the group B streptococcus (GBS) surface immunogenic protein (Sip) at the surface of intact GBS cells were studied by flow cytometric assay and immunogold electron microscopy [23].
• In addition, active immunization with purified recombinant Sip protein of female CD-1 mice induced the production of specific antibodies that also confer protection to the newborn pups against GBS strains of serotypes Ia/c, Ib, II, III, and V [5].
• Using ELISA, most (99%) women and newborns (97%) had serum Sip antibodies, as did most newborns followed through 6 months [36].
• Stress-induced hyperthermia in mice: a methodological study [37].

References