Seroatlas · Human Serome Atlas

CINP

Cyclin-dependent kinase 2-interacting protein

Also known as: CINP_HUMAN, MGC849

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession: Q9BW66
Gene: CINP
Ensembl: ENSG00000100865
Chromosome: 14
Canonical length: 212 aa
Protein class: Metabolic proteins, Predicted intracellular proteins
Quaternary structure: Homodimer

OverviewNCBI Gene

The protein encoded by this gene is reported to be a component of the DNA replication complex as well as a genome-maintenance protein. It may interact with proteins important for replication initiation and has been shown to bind chromatin at the G1 phase of the cell cycle and dissociate from chromatin with replication initiation. It may also serve to regulate checkpoint signaling as part of the DNA damage response. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2016]

Canonical amino-acid sequenceUniProt

212 residues, UniProt reviewed canonical sequence.

>Q9BW66|CINP
     1  MEAKTLGTVT PRKPVLSVSA RKIKDNAADW HNLILKWETL NDAGFTTANN IANLKISLLN
    61  KDKIELDSSS PASKENEEKV CLEYNEELEK LCEELQATLD GLTKIQVKME KLSSTTKGIC
   121  ELENYHYGEE SKRPPLFHTW PTTHFYEVSH KLLEMYRKEL LLKRTVAKEL AHTGDPDLTL
   181  SYLSMWLHQP YVESDSRLHL ESMLLETGHR AL

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against CINP can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.

Antibody reachability: Intracellular
Secreted: No
Transmembrane segments: 0
Mean surface accessibility (rSASA): 0.34
Highest tissue expression: 42 nTPM

Expression across tissuesHPA

Tissue

pancreas: 42 nTPM
spinal cord: 33 nTPM
liver: 32 nTPM
choroid plexus: 30 nTPM
skeletal muscle: 30 nTPM
salivary gland: 28 nTPM

Single-cell type

late primary spermatocytes: 192 nCPM
late spermatids: 174 nCPM
oocytes: 134 nCPM
esophageal suprabasal cells: 122 nCPM
esophageal basal cells: 90 nCPM
esophageal apical cells: 90 nCPM

Immune cell

classical monocyte: 59 nTPM
intermediate monocyte: 59 nTPM
eosinophil: 55 nTPM
myeloid DC: 54 nTPM
non-classical monocyte: 51 nTPM
plasmacytoid DC: 51 nTPM

Brain region

white matter: 25 nTPM
cerebellum: 22 nTPM
basal ganglia: 20 nTPM
spinal cord: 20 nTPM
pons: 20 nTPM
medulla oblongata: 19 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about CINP.

Disease | GeneticClinVar

1 pathogenic / likely-pathogenic of 10 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

Genetic constraint and essentialitygnomAD · DepMap

Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.

gnomAD LOEUF (loss-of-function intolerance): 0.78
gnomAD pLI: 0.06
gnomAD missense Z: 0.51
DepMap mean gene effect: -0.96
DepMap dependency class: common

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

preribosome binding

Cellular components

nucleus

Protein domainsUniProt · Pfam · InterPro

Cyclin-dependent kinase 2-interacting protein

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of CINP in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads CINP as an antibody target. Whether an autoantibody or antibody against CINP could matter depends on whether native CINP is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

CINP is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.

Annotation status

The present source text does not explicitly label CINP as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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