IMP2 Inner Mitochondrial Membrane Peptidase-Like (S. Cerevisiae) (IMMP2L) ELISA Kits

Human IMP2 Inner Mitochondrial Membrane Peptidase-Like (S. Cerevisiae) (IMMP2L) interaction partners

1. While the IMMP2L deletions carried non-recurrent breakpoints, in contrast to previous reports, meta-analysis found no evidence of association (P > 0.05) between IMMP2L deletions and ASD. We also observed common exonic deletions impacting IMMP2L in a separate control (5,971 samples) cohort where subjects were screened for psychiatric conditions.

2. data would indicate that deletions involving the IMMP2L gene may contribute to the development of a subgroup of cognitive/behavioral disorders

3. Deficiency of IMMP2L in cells cultured under hypoxia and high glucose, exacerbated neuronal death.

4. Chromosomal breakpoints involved the IMMP2L gene in 7q31 is associated with Diffuse Large B-Cell Lymphomas.

5. IMMP2L transcription requires Topoisomerase I in human primary astrocytes

6. genomic rearrangements affecting IMMP2L may be one of the predisposing factors involved in Tourette syndrome and overlapping neurodevelopmental disorders.

7. Five genes have been directly disrupted in Tourette Syndrome by independent genomic rearrangements and copy number variations with unique breakpoints.

8. AUTS1/AUTS5 linkage to immp2l-dock4 may be involved in autism susceptibility

Mouse (Murine) IMP2 Inner Mitochondrial Membrane Peptidase-Like (S. Cerevisiae) (IMMP2L) interaction partners

1. IMP2-deficient muscle exhibits reduced fatty acid oxidation, due to a reduced abundance of mRNA of peroxisome proliferator-activated receptor alpha (PPARalpha), an IMP2 client, and PPARalpha protein. IMP2-deficient muscle fibers treated with a mitochondrial uncoupler to increase electron flux, as occurs with exercise, exhibit reduced oxygen consumption from fatty acids, with higher oxygen consumption from glucose.

2. Data indicates that overexpression of IMP2 alters the regulatory capacity of many miRNAs and conclude that IMP2 competes with miRNAs for binding sites on thousands of transcripts. As a result, data implicates that overexpression of IMP2 has distinct effects to the regulatory capacity of miRNAs with yet unknown consequences for translational efficiency.

3. The results indicate that IMP2 deficiency delayed bone remodeling by significantly inhibiting the activity of osteoclasts and impairing their adhesion.

4. data suggest that respiratory deficiency is not the cause of the observed Immp2l mutant phenotypes.

5. provides evidence for a causal role of oxidative stress in neurodegeneration of Immp2l mutant mice

6. IMP2 as a developmental stage-dependent regulator of the differentiation potentials of NPCs in the mouse neocortex.

7. This study demomistrated that Immp2l deficiency increases ischemic brain damage by enhancing O(2)(-) production and damaging mitochondrial functional performance.

8. Mitochondrial peptidase IMMP2L mutation causes early onset of age-associated disorders and impairs adult stem cell self-renewal