3.1.3.56 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27750211/ INPP5D rs35349669 polymorphism with late-onset Alzheimer's disease: A replication study and meta-analysis. causal interaction 4 3.1.3.56 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27750211/ INPP5D rs35349669 polymorphism with late-onset Alzheimer's disease: A replication study and meta-analysis. diagnostic usage 3 3.1.3.56 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27750211/ INPP5D rs35349669 polymorphism with late-onset Alzheimer's disease: A replication study and meta-analysis. ongoing research 1 3.1.3.56 Alzheimer Disease https://pubmed.ncbi.nlm.nih.gov/27750211/ INPP5D rs35349669 polymorphism with late-onset Alzheimer's disease: A replication study and meta-analysis. unassigned - 3.1.3.56 Astrocytoma https://pubmed.ncbi.nlm.nih.gov/24358143/ Identification of novel genetic alterations in samples of malignant glioma patients. ongoing research 2 3.1.3.56 Astrocytoma https://pubmed.ncbi.nlm.nih.gov/24358143/ Identification of novel genetic alterations in samples of malignant glioma patients. unassigned - 3.1.3.56 Ataxia https://pubmed.ncbi.nlm.nih.gov/26051944/ Deletion of Inpp5a causes ataxia and cerebellar degeneration in mice. causal interaction 2 3.1.3.56 Ataxia https://pubmed.ncbi.nlm.nih.gov/33792664/ INPP5K and SIL1 associated pathologies with overlapping clinical phenotypes converge through dysregulation of PHGDH. causal interaction 4 3.1.3.56 Ataxia https://pubmed.ncbi.nlm.nih.gov/26051944/ Deletion of Inpp5a causes ataxia and cerebellar degeneration in mice. unassigned - 3.1.3.56 Ataxia https://pubmed.ncbi.nlm.nih.gov/33792664/ INPP5K and SIL1 associated pathologies with overlapping clinical phenotypes converge through dysregulation of PHGDH. unassigned - 3.1.3.56 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28448505/ Polyphenolic extract of InsP 5-ptase expressing tomato plants reduce the proliferation of MCF-7 breast cancer cells. diagnostic usage 3 3.1.3.56 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28448505/ Polyphenolic extract of InsP 5-ptase expressing tomato plants reduce the proliferation of MCF-7 breast cancer cells. therapeutic application 1 3.1.3.56 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28448505/ Polyphenolic extract of InsP 5-ptase expressing tomato plants reduce the proliferation of MCF-7 breast cancer cells. ongoing research 3 3.1.3.56 Breast Neoplasms https://pubmed.ncbi.nlm.nih.gov/28448505/ Polyphenolic extract of InsP 5-ptase expressing tomato plants reduce the proliferation of MCF-7 breast cancer cells. unassigned - 3.1.3.56 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. causal interaction 4 3.1.3.56 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. diagnostic usage 4 3.1.3.56 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. therapeutic application 1 3.1.3.56 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25759212/ A distinct and replicable variant of the squamous cell carcinoma gene inositol polyphosphate-5-phosphatase modifies the susceptibility of arsenic-associated skin lesions in Bangladesh. ongoing research 1 3.1.3.56 Carcinoma https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. ongoing research 3 3.1.3.56 Carcinoma https://pubmed.ncbi.nlm.nih.gov/19875416/ Random DNA fragmentation allows detection of single-copy, single-exon alterations of copy number by oligonucleotide array CGH in clinical FFPE samples. ongoing research 3 3.1.3.56 Carcinoma https://pubmed.ncbi.nlm.nih.gov/25759212/ A distinct and replicable variant of the squamous cell carcinoma gene inositol polyphosphate-5-phosphatase modifies the susceptibility of arsenic-associated skin lesions in Bangladesh. unassigned - 3.1.3.56 Carcinoma https://pubmed.ncbi.nlm.nih.gov/28696004/ Frequent loss of inositol polyphosphate-5-phosphatase in oropharyngeal squamous cell carcinoma. unassigned - 3.1.3.56 Carcinoma https://pubmed.ncbi.nlm.nih.gov/19875416/ Random DNA fragmentation allows detection of single-copy, single-exon alterations of copy number by oligonucleotide array CGH in clinical FFPE samples. unassigned - 3.1.3.56 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. causal interaction 4 3.1.3.56 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. diagnostic usage 4 3.1.3.56 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. therapeutic application 1 3.1.3.56 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/25759212/ A distinct and replicable variant of the squamous cell carcinoma gene inositol polyphosphate-5-phosphatase modifies the susceptibility of arsenic-associated skin lesions in Bangladesh. ongoing research 1 3.1.3.56 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. ongoing research 3 3.1.3.56 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/19875416/ Random DNA fragmentation allows detection of single-copy, single-exon alterations of copy number by oligonucleotide array CGH in clinical FFPE samples. ongoing research 3 3.1.3.56 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/25759212/ A distinct and replicable variant of the squamous cell carcinoma gene inositol polyphosphate-5-phosphatase modifies the susceptibility of arsenic-associated skin lesions in Bangladesh. unassigned - 3.1.3.56 Carcinoma, Squamous Cell https://pubmed.ncbi.nlm.nih.gov/19875416/ Random DNA fragmentation allows detection of single-copy, single-exon alterations of copy number by oligonucleotide array CGH in clinical FFPE samples. unassigned - 3.1.3.56 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/19875726/ Inpp5f Is a Polyphosphoinositide Phosphatase That Regulates Cardiac Hypertrophic Responsiveness. causal interaction 3 3.1.3.56 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/19875726/ Inpp5f Is a Polyphosphoinositide Phosphatase That Regulates Cardiac Hypertrophic Responsiveness. ongoing research 2 3.1.3.56 Cardiomegaly https://pubmed.ncbi.nlm.nih.gov/19875726/ Inpp5f Is a Polyphosphoinositide Phosphatase That Regulates Cardiac Hypertrophic Responsiveness. unassigned - 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/28190456/ Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment. causal interaction 4 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/28940338/ INPP5K variant causes autosomal recessive congenital cataract in a Pakistani family. causal interaction 4 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/33193651/ A Recurrent Pathogenic Variant of INPP5K Underlies Autosomal Recessive Congenital Muscular Dystrophy With Cataracts and Intellectual Disability: Evidence for a Founder Effect in Southern Italy. causal interaction 4 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. causal interaction 3 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. causal interaction 4 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/33792664/ INPP5K and SIL1 associated pathologies with overlapping clinical phenotypes converge through dysregulation of PHGDH. causal interaction 4 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/28940338/ INPP5K variant causes autosomal recessive congenital cataract in a Pakistani family. diagnostic usage 3 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/28190456/ Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment. therapeutic application 1 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/33193651/ A Recurrent Pathogenic Variant of INPP5K Underlies Autosomal Recessive Congenital Muscular Dystrophy With Cataracts and Intellectual Disability: Evidence for a Founder Effect in Southern Italy. therapeutic application 1 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. therapeutic application 1 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. ongoing research 3 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/28190456/ Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment. unassigned - 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/33193651/ A Recurrent Pathogenic Variant of INPP5K Underlies Autosomal Recessive Congenital Muscular Dystrophy With Cataracts and Intellectual Disability: Evidence for a Founder Effect in Southern Italy. unassigned - 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. unassigned - 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. unassigned - 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/33792664/ INPP5K and SIL1 associated pathologies with overlapping clinical phenotypes converge through dysregulation of PHGDH. unassigned - 3.1.3.56 Cataract https://pubmed.ncbi.nlm.nih.gov/28940338/ INPP5K variant causes autosomal recessive congenital cataract in a Pakistani family. unassigned - 3.1.3.56 Ciliopathies https://pubmed.ncbi.nlm.nih.gov/19668216/ Mutations in INPP5E, encoding inositol polyphosphate-5-phosphatase E, link phosphatidyl inositol signaling to the ciliopathies. unassigned - 3.1.3.56 Dehydration https://pubmed.ncbi.nlm.nih.gov/22573619/ Inositol polyphosphate 5-phosphatase-controlled Ins(1,4,5)P3/Ca2+ is crucial for maintaining pollen dormancy and regulating early germination of pollen. therapeutic application 1 3.1.3.56 Dehydration https://pubmed.ncbi.nlm.nih.gov/22573619/ Inositol polyphosphate 5-phosphatase-controlled Ins(1,4,5)P3/Ca2+ is crucial for maintaining pollen dormancy and regulating early germination of pollen. unassigned - 3.1.3.56 Genetic Diseases, Inborn https://pubmed.ncbi.nlm.nih.gov/23389333/ Novel OCRL mutations in Chinese children with Lowe syndrome. causal interaction 4 3.1.3.56 Genetic Diseases, Inborn https://pubmed.ncbi.nlm.nih.gov/23389333/ Novel OCRL mutations in Chinese children with Lowe syndrome. unassigned - 3.1.3.56 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/24358143/ Identification of novel genetic alterations in samples of malignant glioma patients. ongoing research 2 3.1.3.56 Glioblastoma https://pubmed.ncbi.nlm.nih.gov/24358143/ Identification of novel genetic alterations in samples of malignant glioma patients. unassigned - 3.1.3.56 Glioma https://pubmed.ncbi.nlm.nih.gov/25476455/ Inositol Polyphosphate-5-Phosphatase F (INPP5F) inhibits STAT3 activity and suppresses gliomas tumorigenicity. causal interaction 4 3.1.3.56 Glioma https://pubmed.ncbi.nlm.nih.gov/25476455/ Inositol Polyphosphate-5-Phosphatase F (INPP5F) inhibits STAT3 activity and suppresses gliomas tumorigenicity. diagnostic usage 3 3.1.3.56 Glioma https://pubmed.ncbi.nlm.nih.gov/25476455/ Inositol Polyphosphate-5-Phosphatase F (INPP5F) inhibits STAT3 activity and suppresses gliomas tumorigenicity. therapeutic application 4 3.1.3.56 Glioma https://pubmed.ncbi.nlm.nih.gov/24358143/ Identification of novel genetic alterations in samples of malignant glioma patients. ongoing research 2 3.1.3.56 Glioma https://pubmed.ncbi.nlm.nih.gov/24358143/ Identification of novel genetic alterations in samples of malignant glioma patients. unassigned - 3.1.3.56 Glioma https://pubmed.ncbi.nlm.nih.gov/25476455/ Inositol Polyphosphate-5-Phosphatase F (INPP5F) inhibits STAT3 activity and suppresses gliomas tumorigenicity. unassigned - 3.1.3.56 inositol-polyphosphate 5-phosphatase deficiency https://pubmed.ncbi.nlm.nih.gov/2567894/ Inositol 1,4,5-trisphosphate phosphatase deficiency and malignant hyperpyrexia in swine. causal interaction 3 3.1.3.56 inositol-polyphosphate 5-phosphatase deficiency https://pubmed.ncbi.nlm.nih.gov/2567894/ Inositol 1,4,5-trisphosphate phosphatase deficiency and malignant hyperpyrexia in swine. unassigned - 3.1.3.56 Insulin Resistance https://pubmed.ncbi.nlm.nih.gov/26483413/ Phosphatidylinositol 3,4,5-Trisphosphate Phosphatase SKIP Links Endoplasmic Reticulum Stress in Skeletal Muscle to Insulin Resistance. ongoing research 4 3.1.3.56 Insulin Resistance https://pubmed.ncbi.nlm.nih.gov/26483413/ Phosphatidylinositol 3,4,5-Trisphosphate Phosphatase SKIP Links Endoplasmic Reticulum Stress in Skeletal Muscle to Insulin Resistance. unassigned - 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/33193651/ A Recurrent Pathogenic Variant of INPP5K Underlies Autosomal Recessive Congenital Muscular Dystrophy With Cataracts and Intellectual Disability: Evidence for a Founder Effect in Southern Italy. causal interaction 4 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28190456/ Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment. causal interaction 4 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. causal interaction 3 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28940338/ INPP5K variant causes autosomal recessive congenital cataract in a Pakistani family. causal interaction 4 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. causal interaction 4 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28940338/ INPP5K variant causes autosomal recessive congenital cataract in a Pakistani family. diagnostic usage 3 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/33193651/ A Recurrent Pathogenic Variant of INPP5K Underlies Autosomal Recessive Congenital Muscular Dystrophy With Cataracts and Intellectual Disability: Evidence for a Founder Effect in Southern Italy. therapeutic application 1 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28190456/ Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment. therapeutic application 1 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. therapeutic application 1 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. ongoing research 3 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/33193651/ A Recurrent Pathogenic Variant of INPP5K Underlies Autosomal Recessive Congenital Muscular Dystrophy With Cataracts and Intellectual Disability: Evidence for a Founder Effect in Southern Italy. unassigned - 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28190456/ Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment. unassigned - 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. unassigned - 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. unassigned - 3.1.3.56 Intellectual Disability https://pubmed.ncbi.nlm.nih.gov/28940338/ INPP5K variant causes autosomal recessive congenital cataract in a Pakistani family. unassigned - 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/20876729/ Loss of inositol polyphosphate 5-phosphatase is an early event in development of cutaneous squamous cell carcinoma. causal interaction 4 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. causal interaction 4 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. causal interaction 4 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/20876729/ Loss of inositol polyphosphate 5-phosphatase is an early event in development of cutaneous squamous cell carcinoma. diagnostic usage 3 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. diagnostic usage 4 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. diagnostic usage 4 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. therapeutic application 2 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. therapeutic application 1 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/20876729/ Loss of inositol polyphosphate 5-phosphatase is an early event in development of cutaneous squamous cell carcinoma. ongoing research 4 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. ongoing research 3 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. ongoing research 3 3.1.3.56 Keratosis, Actinic https://pubmed.ncbi.nlm.nih.gov/20876729/ Loss of inositol polyphosphate 5-phosphatase is an early event in development of cutaneous squamous cell carcinoma. unassigned - 3.1.3.56 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32420386/ The Prediction and Prognostic Significance of INPP5K Expression in Patients with Liver Cancer. causal interaction 4 3.1.3.56 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32420386/ The Prediction and Prognostic Significance of INPP5K Expression in Patients with Liver Cancer. diagnostic usage 4 3.1.3.56 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32420386/ The Prediction and Prognostic Significance of INPP5K Expression in Patients with Liver Cancer. ongoing research 4 3.1.3.56 Liver Neoplasms https://pubmed.ncbi.nlm.nih.gov/32420386/ The Prediction and Prognostic Significance of INPP5K Expression in Patients with Liver Cancer. unassigned - 3.1.3.56 Microcephaly https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. causal interaction 3 3.1.3.56 Microcephaly https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. therapeutic application 1 3.1.3.56 Microcephaly https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. unassigned - 3.1.3.56 Microphthalmos https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. causal interaction 3 3.1.3.56 Microphthalmos https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. therapeutic application 1 3.1.3.56 Microphthalmos https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. unassigned - 3.1.3.56 Muscular Diseases https://pubmed.ncbi.nlm.nih.gov/33792664/ INPP5K and SIL1 associated pathologies with overlapping clinical phenotypes converge through dysregulation of PHGDH. causal interaction 4 3.1.3.56 Muscular Diseases https://pubmed.ncbi.nlm.nih.gov/33792664/ INPP5K and SIL1 associated pathologies with overlapping clinical phenotypes converge through dysregulation of PHGDH. unassigned - 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/28190456/ Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment. causal interaction 4 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. causal interaction 3 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/33193651/ A Recurrent Pathogenic Variant of INPP5K Underlies Autosomal Recessive Congenital Muscular Dystrophy With Cataracts and Intellectual Disability: Evidence for a Founder Effect in Southern Italy. causal interaction 4 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/28940338/ INPP5K variant causes autosomal recessive congenital cataract in a Pakistani family. causal interaction 4 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. causal interaction 4 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/33879025/ Bidirectional interconversion between PtdIns4P and PtdIns(4,5)P2 is required for autophagic lysosome reformation and protection from skeletal muscle disease. causal interaction 4 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/28940338/ INPP5K variant causes autosomal recessive congenital cataract in a Pakistani family. diagnostic usage 3 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/28190456/ Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment. therapeutic application 1 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. therapeutic application 1 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/33193651/ A Recurrent Pathogenic Variant of INPP5K Underlies Autosomal Recessive Congenital Muscular Dystrophy With Cataracts and Intellectual Disability: Evidence for a Founder Effect in Southern Italy. therapeutic application 1 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. ongoing research 3 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/33119550/ Defective lysosome reformation during autophagy causes skeletal muscle disease. unassigned - 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/28190456/ Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment. unassigned - 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/28190459/ Mutations in INPP5K Cause a Form of Congenital Muscular Dystrophy Overlapping Marinesco-Sjögren Syndrome and Dystroglycanopathy. unassigned - 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/33193651/ A Recurrent Pathogenic Variant of INPP5K Underlies Autosomal Recessive Congenital Muscular Dystrophy With Cataracts and Intellectual Disability: Evidence for a Founder Effect in Southern Italy. unassigned - 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. unassigned - 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/33879025/ Bidirectional interconversion between PtdIns4P and PtdIns(4,5)P2 is required for autophagic lysosome reformation and protection from skeletal muscle disease. unassigned - 3.1.3.56 Muscular Dystrophies https://pubmed.ncbi.nlm.nih.gov/28940338/ INPP5K variant causes autosomal recessive congenital cataract in a Pakistani family. unassigned - 3.1.3.56 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. causal interaction 4 3.1.3.56 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33798953/ A new gene panel as a marker for ESCC poor prognosis; INPP5A, TWIST1, MMP2, and EGFR. causal interaction 4 3.1.3.56 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. diagnostic usage 4 3.1.3.56 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. therapeutic application 2 3.1.3.56 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. ongoing research 3 3.1.3.56 Neoplasm Metastasis https://pubmed.ncbi.nlm.nih.gov/33798953/ A new gene panel as a marker for ESCC poor prognosis; INPP5A, TWIST1, MMP2, and EGFR. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26170120/ Analysis of an independent tumor suppressor locus telomeric to Tp53 suggested Inpp5k and Myo1c as novel tumor suppressor gene candidates in this region. causal interaction 3 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20876729/ Loss of inositol polyphosphate 5-phosphatase is an early event in development of cutaneous squamous cell carcinoma. causal interaction 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25448479/ Engineering PTEN function: Membrane association and activity. causal interaction 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25955013/ Canine Mammary Tumours Are Affected by Frequent Copy Number Aberrations, including Amplification of MYC and Loss of PTEN. causal interaction 2 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26282217/ MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression. causal interaction 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28653606/ MiR-181a-5p Promotes Proliferation and Invasion, and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). causal interaction 1 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. causal interaction 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. causal interaction 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32420386/ The Prediction and Prognostic Significance of INPP5K Expression in Patients with Liver Cancer. causal interaction 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. causal interaction 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33488112/ The Prognostic Value of DNA Methylation, Post-Translational Modifications and Correlated with Immune Infiltrates in Gynecologic Cancers. causal interaction 3 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33798953/ A new gene panel as a marker for ESCC poor prognosis; INPP5A, TWIST1, MMP2, and EGFR. causal interaction 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20876729/ Loss of inositol polyphosphate 5-phosphatase is an early event in development of cutaneous squamous cell carcinoma. diagnostic usage 3 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. diagnostic usage 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. diagnostic usage 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32420386/ The Prediction and Prognostic Significance of INPP5K Expression in Patients with Liver Cancer. diagnostic usage 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33488112/ The Prognostic Value of DNA Methylation, Post-Translational Modifications and Correlated with Immune Infiltrates in Gynecologic Cancers. diagnostic usage 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/14996095/ SEREX identification of new tumour-associated antigens in cutaneous T-cell lymphoma. therapeutic application 1 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26282217/ MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression. therapeutic application 2 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28653606/ MiR-181a-5p Promotes Proliferation and Invasion, and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). therapeutic application 2 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. therapeutic application 2 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. therapeutic application 1 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19875416/ Random DNA fragmentation allows detection of single-copy, single-exon alterations of copy number by oligonucleotide array CGH in clinical FFPE samples. ongoing research 3 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20876729/ Loss of inositol polyphosphate 5-phosphatase is an early event in development of cutaneous squamous cell carcinoma. ongoing research 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26282217/ MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression. ongoing research 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28653606/ MiR-181a-5p Promotes Proliferation and Invasion, and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). ongoing research 2 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/30359624/ The prognostic value of inositol polyphosphate 5-phosphatase in cutaneous squamous cell carcinoma. ongoing research 3 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/31437542/ Prognostic Value of Inositol Polyphosphate-5-Phosphatase Expression in Recurrent and Metastatic Cutaneous Squamous Cell Carcinoma. ongoing research 3 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32420386/ The Prediction and Prognostic Significance of INPP5K Expression in Patients with Liver Cancer. ongoing research 4 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. ongoing research 3 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/14996095/ SEREX identification of new tumour-associated antigens in cutaneous T-cell lymphoma. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/19875416/ Random DNA fragmentation allows detection of single-copy, single-exon alterations of copy number by oligonucleotide array CGH in clinical FFPE samples. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/23853711/ Phosphorylation-mediated PTEN conformational closure and deactivation revealed with protein semisynthesis. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26170120/ Analysis of an independent tumor suppressor locus telomeric to Tp53 suggested Inpp5k and Myo1c as novel tumor suppressor gene candidates in this region. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25448479/ Engineering PTEN function: Membrane association and activity. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/25955013/ Canine Mammary Tumours Are Affected by Frequent Copy Number Aberrations, including Amplification of MYC and Loss of PTEN. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/26282217/ MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/28653606/ MiR-181a-5p Promotes Proliferation and Invasion, and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33060052/ The phosphoinositide 5-phosphatase INPP5K: From gene structure to in vivo functions. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33798953/ A new gene panel as a marker for ESCC poor prognosis; INPP5A, TWIST1, MMP2, and EGFR. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/20876729/ Loss of inositol polyphosphate 5-phosphatase is an early event in development of cutaneous squamous cell carcinoma. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/32420386/ The Prediction and Prognostic Significance of INPP5K Expression in Patients with Liver Cancer. unassigned - 3.1.3.56 Neoplasms https://pubmed.ncbi.nlm.nih.gov/33488112/ The Prognostic Value of DNA Methylation, Post-Translational Modifications and Correlated with Immune Infiltrates in Gynecologic Cancers. unassigned - 3.1.3.56 Neural Tube Defects https://pubmed.ncbi.nlm.nih.gov/29626185/ Relationship Between INPP5E Gene Expression and Embryonic Neural Development in a Mouse Model of Neural Tube Defect. causal interaction 1 3.1.3.56 Neural Tube Defects https://pubmed.ncbi.nlm.nih.gov/29626185/ Relationship Between INPP5E Gene Expression and Embryonic Neural Development in a Mouse Model of Neural Tube Defect. ongoing research 4 3.1.3.56 Neural Tube Defects https://pubmed.ncbi.nlm.nih.gov/29626185/ Relationship Between INPP5E Gene Expression and Embryonic Neural Development in a Mouse Model of Neural Tube Defect. unassigned - 3.1.3.56 Oculocerebrorenal Syndrome https://pubmed.ncbi.nlm.nih.gov/23389333/ Novel OCRL mutations in Chinese children with Lowe syndrome. causal interaction 4 3.1.3.56 Oculocerebrorenal Syndrome https://pubmed.ncbi.nlm.nih.gov/23692838/ A novel OCRL1 gene mutation in a Turkish child with Lowe syndrome. causal interaction 3 3.1.3.56 Oculocerebrorenal Syndrome https://pubmed.ncbi.nlm.nih.gov/24614960/ A Novel OCRL1 Mutation in a Patient with the Mild Phenotype of Lowe Syndrome. causal interaction 4 3.1.3.56 Oculocerebrorenal Syndrome https://pubmed.ncbi.nlm.nih.gov/23692838/ A novel OCRL1 gene mutation in a Turkish child with Lowe syndrome. therapeutic application 1 3.1.3.56 Oculocerebrorenal Syndrome https://pubmed.ncbi.nlm.nih.gov/1321346/ The Lowe's oculocerebrorenal syndrome gene encodes a protein highly homologous to inositol polyphosphate-5-phosphatase. unassigned - 3.1.3.56 Oculocerebrorenal Syndrome https://pubmed.ncbi.nlm.nih.gov/27766457/ Decreased urinary excretion of the ectodomain form of megalin (A-megalin) in children with OCRL gene mutations. unassigned - 3.1.3.56 Oculocerebrorenal Syndrome https://pubmed.ncbi.nlm.nih.gov/23389333/ Novel OCRL mutations in Chinese children with Lowe syndrome. unassigned - 3.1.3.56 Oculocerebrorenal Syndrome https://pubmed.ncbi.nlm.nih.gov/23692838/ A novel OCRL1 gene mutation in a Turkish child with Lowe syndrome. unassigned - 3.1.3.56 Oculocerebrorenal Syndrome https://pubmed.ncbi.nlm.nih.gov/24614960/ A Novel OCRL1 Mutation in a Patient with the Mild Phenotype of Lowe Syndrome. unassigned - 3.1.3.56 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/26282217/ MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression. causal interaction 4 3.1.3.56 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/26282217/ MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression. therapeutic application 2 3.1.3.56 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/26282217/ MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression. ongoing research 4 3.1.3.56 Ovarian Neoplasms https://pubmed.ncbi.nlm.nih.gov/26282217/ MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression. unassigned - 3.1.3.56 Parkinson Disease https://pubmed.ncbi.nlm.nih.gov/29607885/ Association analysis of NUCKS1 and INPP5K polymorphism with Parkinson's disease. causal interaction 2 3.1.3.56 Parkinson Disease https://pubmed.ncbi.nlm.nih.gov/30225765/ Parkinson's Disease Risk Variant rs1109303 Regulates the Expression of INPP5K and CRK in Human Brain. diagnostic usage 3 3.1.3.56 Parkinson Disease https://pubmed.ncbi.nlm.nih.gov/30225765/ Parkinson's Disease Risk Variant rs1109303 Regulates the Expression of INPP5K and CRK in Human Brain. ongoing research 1 3.1.3.56 Parkinson Disease https://pubmed.ncbi.nlm.nih.gov/30225765/ Parkinson's Disease Risk Variant rs1109303 Regulates the Expression of INPP5K and CRK in Human Brain. unassigned - 3.1.3.56 Parkinson Disease https://pubmed.ncbi.nlm.nih.gov/29607885/ Association analysis of NUCKS1 and INPP5K polymorphism with Parkinson's disease. unassigned - 3.1.3.56 phosphoinositide 5-phosphatase deficiency https://pubmed.ncbi.nlm.nih.gov/19736566/ The role of Arabidopsis 5PTase13 in root gravitropism through modulation of vesicle trafficking. causal interaction 2 3.1.3.56 phosphoinositide 5-phosphatase deficiency https://pubmed.ncbi.nlm.nih.gov/19736566/ The role of Arabidopsis 5PTase13 in root gravitropism through modulation of vesicle trafficking. unassigned - 3.1.3.56 Spinocerebellar Ataxias https://pubmed.ncbi.nlm.nih.gov/32107387/ Cerebellum-enriched protein INPP5A contributes to selective neuropathology in mouse model of spinocerebellar ataxias type 17. therapeutic application 1 3.1.3.56 Spinocerebellar Ataxias https://pubmed.ncbi.nlm.nih.gov/32107387/ Cerebellum-enriched protein INPP5A contributes to selective neuropathology in mouse model of spinocerebellar ataxias type 17. unassigned - 3.1.3.56 Squamous Cell Carcinoma of Head and Neck https://pubmed.ncbi.nlm.nih.gov/28696004/ Frequent loss of inositol polyphosphate-5-phosphatase in oropharyngeal squamous cell carcinoma. unassigned - 3.1.3.56 Thymoma https://pubmed.ncbi.nlm.nih.gov/17322895/ Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity. causal interaction 4 3.1.3.56 Thymoma https://pubmed.ncbi.nlm.nih.gov/17322895/ Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity. therapeutic application 4 3.1.3.56 Thymoma https://pubmed.ncbi.nlm.nih.gov/17322895/ Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity. unassigned - 3.1.3.56 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/28653606/ MiR-181a-5p Promotes Proliferation and Invasion, and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). causal interaction 1 3.1.3.56 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/28653606/ MiR-181a-5p Promotes Proliferation and Invasion, and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). therapeutic application 2 3.1.3.56 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/28653606/ MiR-181a-5p Promotes Proliferation and Invasion, and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). ongoing research 2 3.1.3.56 Uterine Cervical Neoplasms https://pubmed.ncbi.nlm.nih.gov/28653606/ MiR-181a-5p Promotes Proliferation and Invasion, and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A). unassigned -