Disease on EC 3.4.23.36 - Signal peptidase II
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DISEASE 
TITLE OF PUBLICATION
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Alzheimer Disease
Exome-wide age-of-onset analysis reveals exonic variants in ERN1 and SPPL2C associated with Alzheimer's disease.
Arthritis, Psoriatic
Impaired proteolysis by SPPL2a causes CD74 fragment accumulation that can be recognized by anti-CD74 autoantibodies in human ankylosing spondylitis.
Arthritis, Rheumatoid
Impaired proteolysis by SPPL2a causes CD74 fragment accumulation that can be recognized by anti-CD74 autoantibodies in human ankylosing spondylitis.
Autoimmune Diseases
Discovery of the First Potent, Selective, and Orally Bioavailable Signal Peptide Peptidase-Like 2a (SPPL2a) Inhibitor Displaying Pronounced Immunomodulatory Effects In Vivo.
Autoimmune Diseases
Identification of SPPL2a Inhibitors by Multiparametric Analysis of a High-Content Ultra-High-Throughput Screen.
Autoimmune Diseases
The association of clinical phenotypes to known AD/FTD genetic risk loci and their inter-relationship.
Ehrlichiosis
Proteomic analysis of and immune responses to Ehrlichia chaffeensis lipoproteins.
Frontotemporal Lobar Degeneration
Regulated intramembrane proteolysis of the frontotemporal lobar degeneration risk factor, TMEM106B, by signal peptide peptidase-like 2a (SPPL2a).
Glioblastoma
ODZ1 allows glioblastoma to sustain invasiveness through a Myc-dependent transcriptional upregulation of RhoA.
Infections
LspA inactivation in Mycobacterium tuberculosis results in attenuation without affecting phagosome maturation arrest.
Infections
Proteomic analysis of and immune responses to Ehrlichia chaffeensis lipoproteins.
Mastitis
In the absence of Lgt, lipoproteins are shed from Streptococcus uberis independently of Lsp.
Neoplasms
A genome-wide association study of psoriasis and psoriatic arthritis identifies new disease Loci.
Neoplasms
Non-canonical Shedding of TNF? by SPPL2a Is Determined by the Conformational Flexibility of Its Transmembrane Helix.
Neoplasms
SPPL2a and SPPL2b promote intramembrane proteolysis of TNFalpha in activated dendritic cells to trigger IL-12 production.
signal peptidase ii deficiency
B cell survival, surface BCR and BAFFR expression, CD74 metabolism, and CD8- dendritic cells require the intramembrane endopeptidase SPPL2A.
signal peptidase ii deficiency
Deficiency of the Intramembrane Protease SPPL2a Alters Antimycobacterial Cytokine Responses of Dendritic Cells.
signal peptidase ii deficiency
Disruption of an antimycobacterial circuit between dendritic and helper T cells in human SPPL2a deficiency.
signal peptidase ii deficiency
Mendelian susceptibility to mycobacterial disease: 2014-2018 update.
signal peptidase ii deficiency
Mendelian susceptibility to mycobacterial disease: recent discoveries.
signal peptidase ii deficiency
Processing of CD74 by the Intramembrane Protease SPPL2a Is Critical for B Cell Receptor Signaling in Transitional B Cells.
signal peptidase ii deficiency
The intramembrane protease SPPL2c promotes male germ cell development by cleaving phospholamban.
Spondylitis, Ankylosing
Impaired proteolysis by SPPL2a causes CD74 fragment accumulation that can be recognized by anti-CD74 autoantibodies in human ankylosing spondylitis.
Tuberculosis
Lipoprotein processing is essential for resistance of Mycobacterium tuberculosis to malachite green.
Tuberculosis
Lipoproteins are major targets of the polyclonal human T cell response to Mycobacterium tuberculosis.
Tuberculosis
LspA inactivation in Mycobacterium tuberculosis results in attenuation without affecting phagosome maturation arrest.
Tuberculosis
Potent Inhibition of Macrophage Responses to IFN-{gamma} by Live Virulent Mycobacterium tuberculosis Is Independent of Mature Mycobacterial Lipoproteins but Dependent on TLR2.
Tuberculosis
TLR2-Modulating Lipoproteins of the Mycobacterium tuberculosis Complex Enhance the HIV Infectivity of CD4+ T Cells.
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