Disease relevance of Skull19

• Zfpm2-deficient mice died of congestive heart failure at E13 with a syndrome of tricuspid atresia that includes an absent tricuspid valve, a large ASD, a VSD, an elongated left ventricular outflow tract, rightward displacement of the aortic valve and pulmonic stenosis [1].
• RSOR mRNA and protein expression was assessed by competitive polymerase chain reaction (PCR) and immunoprecipitation methods in embryonic kidneys (day E13 to E17) subjected to high glucose ambience and by Northern and Western blot analyses of kidneys of newborn and 1-week-old mice with hyperglycemia [2].
• However, at E13, the projections from both the vestibular and the acoustic ganglion (i.e, cochlear duct) were both NF-66 positive [3].
• The greatest reduction in frequency of all-trans retinoic acid- or triamcinolone-induced secondary cleft palate was obtained by a single-dose IP administration of methionine at 187 mg/kg to pregnant mice on E13 21 hr [4].
• Intraocular pertussis toxin administered at E13 increased cell death of isthmo-optic neurons by 42%, whereas injections at E19 had no effect [5].

Psychiatry related information on Skull19

• The results suggest that the period between stage 34 (E8) and 39 (E13) is a critical period for afferent neuronal development [6].

High impact information on Skull19

• 5. In contrast, in the fetal liver, definitive erythropoiesis beyond the late progenitor (CFU-E) stage was drastically inhibited by the EpoR mutation, and virtually no definitive erythrocytes were produced in vivo, leading to embryonic death by E13 [7].
• Rb(-/-) cells in the CNS, PNS, and lens underwent inappropriate S-phase entry in the conditional mutants at E13 [8].
• In addition, Ark and GnRH transcripts were detected along the GnRH neuron migratory route in the E13 mouse cribriform plate [9].
• Expression of the Prmt1-betageo fusion gene was greatest along the midline of the neural plate and in the forming head fold from embryonic day 7.5 (E7.5) to E8.5 and in the developing central nervous system from E8.5 to E13 [10].
• Histological sections, paintfill experiments and whole-mount hybridizations reveal no abnormality in inner ear development of Foxi1(-/-) mice before E13 [11].

Chemical compound and disease context of Skull19

• Antibodies to sialic acids prepared against strains B and C of Neisseria meningitidis distinguish different subterminal structures: anti-B reacted with E13 and PO cerebellar cells, and anti-C mostly with cells older than P7 [12].

Biological context of Skull19

• When dissected E13 dental epithelium or mesenchyme were cultured in isolation, apoptotic cells were abundant throughout the tissues, whereas when cultured together, apoptosis was inhibited in both tissues close to their interface indicating that epithelial-mesenchymal tissue interactions prevent apoptosis [13].
• Apoptosis was first detected at bud stage (E12-E13) in the central cells of the invaginating dental epithelium suggesting involvement of cell death in epithelial budding morphogenesis [13].
• Second, we have expressed a dominant-negative form of the type 1 Bmp family receptor Alk6 (Bmpr1b -- Mouse Genome Informatics) in the lens in transgenic mice and shown that an inhibition of primary fiber cell differentiation can be detected at E13 [14].
• The mutant allele is also transcribed in osteoblasts of mandibular bone, again starting precisely with the onset of osteogenesis (day E13/14) [15].
• The results show that the expression of both receptors appears as early as E13 during limb muscle development and parallels the expression of skeletal myosin [16].

Anatomical context of Skull19

• Acetylcholine metabolism has been studied in sister cultures of E13 rat spinal cord cells cultured for 1 to 3 weeks with or without conditioned medium (CM) from rat skeletal muscle cells [17].
• The SPP, which arises from the PVE by E13, is principally the progenitor population to the neuroglial population of the mature neocortex and subjacent cerebral wall [18].
• Among these, the trigeminal ganglion is missing 70% of the normal number of neurons, a deficit which develops during the major period of neurogenesis between embryonic stages (E) 10.5 and E13 [19].
• TuJ1 immunoreactivity first appeared in the proliferative zones of the developing cerebral cortex at E13-E14 as the cortical plate was emerging [20].
• In contrast, when progenitor cells derived from later E13 cortex (during active neurogenesis in vivo) undergo P/N divisions they produce a Nestin(+) progenitor and a Nestin(-) neuronal daughter, and Numb segregates preferentially into the neuronal daughter [21].

Associations of Skull19 with chemical compounds

• This was done by a non-hierarchical bioinformatical clustering of four Serial Analysis of Gene Expression libraries performed on DRG at embryonic day E13, neonatal day P0, adult and adult 3 days post-sciatic nerve section [22].
• 5. Effects of Spry-4 on branching were substantially reversed by removal of doxycycline from the dam at E12.5, but not at E13 [23].
• Using E13 mouse SMG organ cultures, we showed that inhibitors of phosphatidylinositol 3-kinase (PI 3-kinase), wortmannin and LY294002, substantially inhibited branching morphogenesis in SMG [24].
• Replacement of two unique glutamate residues, E9 and E13, from the cytoplasmic amino terminal domain of Cx40 with the corresponding lysine residues from Cx43 eliminated the block by 2 mm spermine, reduced the transjunctional voltage (V(j)) gating sensitivity, and reduced the unitary conductance of this Cx40E9,13K gap junction channel protein [25].
• A dose-dependent fulminant apoptosis was observed in day E13 to E17 kidneys subjected to high glucose ambience [2].

Analytical, diagnostic and therapeutic context of Skull19

• Hamsters rendered arhythmic by SCN ablation were implanted with AH tissue from fetal hamsters (E13-E14, homograft controls) or fetal mice or rats (E15-E17) [26].
• When these cells were microinjected into E12 to E13 metanephroi and then placed in transwell organ culture, ES cell-derived, beta-galactosidase-positive cells were identified in epithelial structures resembling tubules [27].
• Bax was detected by immunohistochemistry in germ cells from bcl-x hypomorph and control testes at E12.5 and E13 [28].
• Immunofluorescence showed that both AChRs and 43K were colocalized in patches by E13, the stage at which intramuscular nerves were first detected [29].
• The COL2A1 and novel cDNA were rare transcripts in the embryonic Kidney. However, Southern blot analyses of representations indicated their up-regulated expressions in E13 kidneys [30].

References