Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OT1XADKG)

DOT Name	KIF-binding protein (KIFBP)
Synonyms	KIF1-binding protein; Kinesin family binding protein
Gene Name	KIFBP
Related Disease	Goldberg-Shprintzen syndrome ( ) Lung cancer ( ) Lung carcinoma ( ) Hirschsprung disease ( ) Inborn error of metabolism ( ) Intellectual disability ( ) Isolated congenital microcephaly ( ) Microlissencephaly ( ) Peripheral neuropathy ( ) Rheumatoid arthritis ( ) Neuroblastoma ( ) Hyperglycemia ( ) Non-insulin dependent diabetes ( ) Obesity ( ) Prediabetes syndrome ( ) Osteoarthritis ( )
UniProt ID	KBP_HUMAN
3D Structure	Download 2D Sequence (FASTA) Download 3D Structure (PDB) Download
PDB ID	6ZPG; 6ZPH; 7RSI; 7RSQ; 7RYP; 7RYQ
Pfam ID	PF12309
Sequence	MANVPWAEVCEKFQAALALSRVELHKNPEKEPYKSKYSARALLEEVKALLGPAPEDEDER PEAEDGPGAGDHALGLPAEVVEPEGPVAQRAVRLAVIEFHLGVNHIDTEELSAGEEHLVK CLRLLRRYRLSHDCISLCIQAQNNLGILWSEREEIETAQAYLESSEALYNQYMKEVGSPP LDPTERFLPEEEKLTEQERSKRFEKVYTHNLYYLAQVYQHLEMFEKAAHYCHSTLKRQLE HNAYHPIEWAINAATLSQFYINKLCFMEARHCLSAANVIFGQTGKISATEDTPEAEGEVP ELYHQRKGEIARCWIKYCLTLMQNAQLSMQDNIGELDLDKQSELRALRKKELDEEESIRK KAVQFGTGELCDAISAVEEKVSYLRPLDFEEARELFLLGQHYVFEAKEFFQIDGYVTDHI EVVQDHSALFKVLAFFETDMERRCKMHKRRIAMLEPLTVDLNPQYYLLVNRQIQFEIAHA YYDMMDLKVAIADRLRDPDSHIVKKINNLNKSALKYYQLFLDSLRDPNKVFPEHIGEDVL RPAMLAKFRVARLYGKIITADPKKELENLATSLEHYKFIVDYCEKHPEAAQEIEVELELS KEMVSLLPTKMERFRTKMALT
Function	Required for organization of axonal microtubules, and axonal outgrowth and maintenance during peripheral and central nervous system development.
Tissue Specificity	Highly expressed in heart, brain, ovary, testis, spinal cord and all specific brain regions examined. Moderate expressed at intermediate level in all other adult tissues examined, as well as in fetal liver and brain. Not expressed in blood leukocytes.

Molecular Interaction Atlas (MIA) of This DOT

16 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance
Goldberg-Shprintzen syndrome	DISCMK4N	Definitive	Autosomal recessive	[1]
Lung cancer	DISCM4YA	Definitive	Genetic Variation	[2]
Lung carcinoma	DISTR26C	Definitive	Genetic Variation	[2]
Hirschsprung disease	DISUUSM1	Strong	Altered Expression	[3]
Inborn error of metabolism	DISO5FAY	Strong	Genetic Variation	[4]
Intellectual disability	DISMBNXP	Strong	Biomarker	[5]
Isolated congenital microcephaly	DISUXHZ6	Strong	Genetic Variation	[6]
Microlissencephaly	DISUCKNT	Strong	Biomarker	[5]
Peripheral neuropathy	DIS7KN5G	Strong	Genetic Variation	[6]
Rheumatoid arthritis	DISTSB4J	Strong	Biomarker	[7]
Neuroblastoma	DISVZBI4	moderate	Altered Expression	[3]
Hyperglycemia	DIS0BZB5	Disputed	Biomarker	[8]
Non-insulin dependent diabetes	DISK1O5Z	Disputed	Biomarker	[8]
Obesity	DIS47Y1K	Disputed	Biomarker	[8]
Prediabetes syndrome	DISH2I53	Disputed	Biomarker	[8]
Osteoarthritis	DIS05URM	Limited	Biomarker	[9]
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Molecular Interaction Atlas (MIA)

MIA Detail

Jump to Detail Molecular Interaction Atlas of This DOT

6 Drug(s) Affected the Gene/Protein Processing of This DOT

Drug Name	Drug ID	Highest Status	Interaction	REF
Valproate	DMCFE9I	Approved	Valproate affects the expression of KIF-binding protein (KIFBP).	[10]
Ciclosporin	DMAZJFX	Approved	Ciclosporin decreases the expression of KIF-binding protein (KIFBP).	[11]
Acetaminophen	DMUIE76	Approved	Acetaminophen increases the expression of KIF-binding protein (KIFBP).	[12]
Cupric Sulfate	DMP0NFQ	Approved	Cupric Sulfate decreases the expression of KIF-binding protein (KIFBP).	[13]
Ivermectin	DMDBX5F	Approved	Ivermectin decreases the expression of KIF-binding protein (KIFBP).	[14]
PMID28460551-Compound-2	DM4DOUB	Patented	PMID28460551-Compound-2 decreases the expression of KIF-binding protein (KIFBP).	[15]
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⏷ Show the Full List of 6 Drug(s)

1 Drug(s) Affected the Post-Translational Modifications of This DOT

Drug Name	Drug ID	Highest Status	Interaction	REF
PMID28870136-Compound-52	DMFDERP	Patented	PMID28870136-Compound-52 decreases the phosphorylation of KIF-binding protein (KIFBP).	[16]
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References

1	Technical standards for the interpretation and reporting of constitutional copy-number variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics (ACMG) and the Clinical Genome Resource (ClinGen). Genet Med. 2020 Feb;22(2):245-257. doi: 10.1038/s41436-019-0686-8. Epub 2019 Nov 6.
2	Prediagnosis weight loss, a stronger factor than BMI, to predict survival in patients with lung cancer.Lung Cancer. 2018 Dec;126:55-63. doi: 10.1016/j.lungcan.2018.07.005. Epub 2018 Jul 5.
3	KBP-cytoskeleton interactions underlie developmental anomalies in Goldberg-Shprintzen syndrome.Hum Mol Genet. 2013 Jun 15;22(12):2387-99. doi: 10.1093/hmg/ddt083. Epub 2013 Feb 19.
4	Cortical brain malformations: effect of clinical, neuroradiological, and modern genetic classification.Arch Neurol. 2008 Mar;65(3):358-66. doi: 10.1001/archneur.65.3.358.
5	Homozygous nonsense mutations in KIAA1279 are associated with malformations of the central and enteric nervous systems. Am J Hum Genet. 2005 Jul;77(1):120-6. doi: 10.1086/431244. Epub 2005 May 9.
6	Multiple Functions of KBP in Neural Development Underlie Brain Anomalies in Goldberg-Shprintzen Syndrome.Front Mol Neurosci. 2019 Nov 1;12:265. doi: 10.3389/fnmol.2019.00265. eCollection 2019.
7	Combining naproxen and a dual amylin and calcitonin receptor agonist improves pain and structural outcomes in the collagen-induced arthritis rat model.Arthritis Res Ther. 2019 Feb 22;21(1):68. doi: 10.1186/s13075-019-1819-9.
8	The Dual Amylin- and Calcitonin-Receptor Agonist KBP-042 Works as Adjunct to Metformin on Fasting Hyperglycemia and HbA1c in a Rat Model of Type 2 Diabetes.J Pharmacol Exp Ther. 2017 Jul;362(1):24-30. doi: 10.1124/jpet.117.241281. Epub 2017 Apr 24.
9	A dual amylin and calcitonin receptor agonist inhibits pain behavior and reduces cartilage pathology in an osteoarthritis rat model.Osteoarthritis Cartilage. 2019 Sep;27(9):1339-1346. doi: 10.1016/j.joca.2019.05.016. Epub 2019 Jun 5.
10	Gene Expression Regulation and Pathway Analysis After Valproic Acid and Carbamazepine Exposure in a Human Embryonic Stem Cell-Based Neurodevelopmental Toxicity Assay. Toxicol Sci. 2015 Aug;146(2):311-20. doi: 10.1093/toxsci/kfv094. Epub 2015 May 15.
11	Integrative "-Omics" analysis in primary human hepatocytes unravels persistent mechanisms of cyclosporine A-induced cholestasis. Chem Res Toxicol. 2016 Dec 19;29(12):2164-2174.
12	Increased mitochondrial ROS formation by acetaminophen in human hepatic cells is associated with gene expression changes suggesting disruption of the mitochondrial electron transport chain. Toxicol Lett. 2015 Apr 16;234(2):139-50.
13	Physiological and toxicological transcriptome changes in HepG2 cells exposed to copper. Physiol Genomics. 2009 Aug 7;38(3):386-401.
14	Quantitative proteomics reveals a broad-spectrum antiviral property of ivermectin, benefiting for COVID-19 treatment. J Cell Physiol. 2021 Apr;236(4):2959-2975. doi: 10.1002/jcp.30055. Epub 2020 Sep 22.
15	Cell-based two-dimensional morphological assessment system to predict cancer drug-induced cardiotoxicity using human induced pluripotent stem cell-derived cardiomyocytes. Toxicol Appl Pharmacol. 2019 Nov 15;383:114761. doi: 10.1016/j.taap.2019.114761. Epub 2019 Sep 15.
16	Quantitative phosphoproteomics reveal cellular responses from caffeine, coumarin and quercetin in treated HepG2 cells. Toxicol Appl Pharmacol. 2022 Aug 15;449:116110. doi: 10.1016/j.taap.2022.116110. Epub 2022 Jun 7.