Annotation inferences using phylogenetic trees
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Proteomic analysis of human parotid gland exosomes by multidimensional protein identification technology (MudPIT).
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Shotgun proteomics catalogued proteins in an exosome-enriched fraction of human parotid saliva; GOA reports CRISPLD1 among those HDA identifications.
"Using MudPIT (multidimensional protein identification technology) mass spectrometry, we catalogued 491 proteins in the exosome fraction of human parotid saliva."
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The authors acknowledge that minor contamination can contribute extracellular proteins to the exosome preparation.
"Alternatively, some minor contamination may have occurred during the isolation procedure of the exosomes."
Nonsyndromic cleft lip and palate: CRISPLD genes and the folate gene pathway connection.
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The study found no significant etiologic contribution from CRISPLD1 variation alone to nonsyndromic cleft lip/palate.
"We show that only one CRISPLD1 SNP, rs1455809, had marginally altered transmission (p=0.05) suggesting that variation in CRISPLD1 alone does not play a significant etiologic role in NSCLP."
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The authors explicitly state that the association results require functional validation.
"These results are intriguing and require both validation and functional studies"
In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine.
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Shotgun proteomics identified approximately 900 proteins in exosome-enriched expressed-prostatic-secretion urine pools; GOA reports CRISPLD1 among those HDA identifications.
"in total, close to 900 proteins were identified in the two EPS-urine exosome pools"
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The study notes that proteins detected in exosome preparations may also be present as soluble proteins.
"some of these proteins could also exist as a soluble form."
CRISPLD1: a novel conserved target in the transition to human heart failure.
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CRISPLD1 loss of function raises systolic calcium transients in human iPSC-derived cardiomyocytes.
"pointing towards higher systolic CaT in KO-CM."
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Loss-of-function and pharmacological-rescue experiments support an inhibitory role for CRISPLD1 in cardiomyocyte calcium cycling.
"This loss-of-function and rescue experiments support the converse argument, that CRISPLD1 plays an inhibitory role in CM Ca2+ cycling."
UniProtKB text export for human CRISPLD1 (Q9H336)
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UniProtKB records CRISPLD1 as a secreted protein.
"CC -!- SUBCELLULAR LOCATION: Secreted {ECO:0000305}."
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CRISPLD1 has a predicted N-terminal signal peptide.
"FT SIGNAL 1..23"
Manual literature and annotation review notes for human CRISPLD1
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The sole molecular-adaptor PAINT seed is mouse Glipr1l1, whose sperm/acrosome context and CAP-only architecture do not support transfer to CRISPLD1.
"The sole PANTHER seed for GO:0060090 is therefore biologically specific to a divergent reproductive CAP paralog and does not support transfer to CRISPLD1"
Manual deep-research synthesis for human CRISPLD1
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Current evidence establishes secretion and regulation of cardiomyocyte calcium transients but does not establish a direct calcium-channel or adaptor activity.
"Its direct biochemical activity and extracellular target are unknown."
Local PANTHER PAINT annotations for the CRISPLD family PTHR31331
Local PANTHER entries for the CRISPLD family PTHR31331
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Human CRISPLD1 is a 500-aa member of CRISPLD1 subfamily SF9.
"Q9H336,Cysteine-rich secretory protein LCCL domain-containing 1,protein,9606,Homo sapiens,Homo sapiens (Human),CRISPLD1,500,PTHR31331:SF9,CYSTEINE-RICH SECRETORY PROTEIN LCCL DOMAIN-CONTAINING 1,True"
Local PANTHER entries for the broad CAP family PTHR10334
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Mouse Glipr1l1 is a 236-aa CAP-family protein.
"Q9DAG6,GLIPR1-like protein 1,protein,10090,Mus musculus,Mus musculus (Mouse),Glipr1l1,236,,,True"
GO-CAM source model for regulation of oolemmal binding multimeric complex formation