motifs/domains
| a N terminal signal peptide |
|
three Ig-C2-like domains |
|
a transmembrane segment (TM1) |
|
cytoplasmic domain with a binding motif to the protein 4.1 family of molecules  |
|
cytoplasmic domain with a type II PSD95/Dlg/ZO-1 (PDZ)-binding motif (BM) for associating with other intracellular proteins |
|
a C-terminal transmembrane domain, and an intracellular type II PDZ binding domain and band 4.1 binding domain |
|
extracellular domain of CADM1 undergoing homophilic or heterophilic interaction with CADM3, PVRL3, and CRTAM (class-I MHC-restricted T cell-associated molecule) |
| basic FUNCTION
| potentially involved in cell-surface recognition during synapse assembly |
|
involved in the suppression of lung tumor formation and metastasis |
|
playing an important role in normal cell-cell interaction |
|
a central effector gene for controlling the biologic aggressiveness of the tumor and that it is an essential biomarker for predicting patient prognosis |
|
plays an important role in meningioma pathogenesis |
|
functions as a glioma tumor suppressor |
|
may be playing a role in normal spermatogenesis |
|
synaptic cell adhesion molecule sufficient for promoting the formation of presynaptic terminals and inducing the functional synapse |
|
mediates nerve-mast cell attachment and communication through homophilic binding |
|
may be involved in hormone secretion from islet cell tumors |
|
involved in regulating epidermal stem cell quiescence and location |
|
selectively involved in endothelial cell migration, suggesting a role in endothelial barrier repair |
|
tumor suppressor, involved in cell adhesion and preferentially inactivated in invasive cancer |
|
involved in the formation of epithelia-like cell structure with EPB41L3 and MPP2, while loss of its function could cause morphological transformation of cancer cells |
|
plays an important role in the formation of the epithelial cell structure with mature cell adhesion |
|
CADM1 complex may play a key role in the formation of the epithelia-like cell structure, whereas inactivation of the components of the complex would be a key step in malignant progression of cancer |
|
negatively regulates the morphological complexity of migrating growth cones |
|
acts in developing neurons to shape migrating growth cones and contributes to the adhesive differentiation of their axo-dendritic contacts |
|
contributes to ERBB4 receptor-mediated control of female sexual development |
|
self-assembles laterally via its extracellular, membrane-proximal immunoglobulin (Ig) domains 2 and 3 |
|
function for CADM1 in suppressing metastasis by sensitizing tumor cells to immune surveillance mechanisms |
|
promotes the formation of presynaptic terminals and induces functional synapses in the central nervous system |
| CELLULAR PROCESS
| cell communication
|
| a component
| forms a tripartite protein complex with EPB41L3 and MPP1, MPP2, MPP3 |
| protein
| intracellular PDZ-domain proteins |
|
associating with MPP3(interaction dependent on the presence of a PDZ-binding motif at the carboxyl terminus of TSLC1) |
|
associates with an actin-binding protein, EPB41L3, and a scaffold protein, membrane protein palmitoylated 3 MPP3, MPP2, MPP1 |
|
recruits NMDA receptors via protein EPB41L3 |
|
interaction with PTK2 (PTK2 is a binding partner and effector in shaping growth cones) |
|
interacting with TIAM1 (cytoplasmic domain of CADM1 directly interacted with the PDZ domain of Tiam1 and induced formation of lamellipodia through Rac activation in HTLV-I-transformed cell lines as well as adult T-cell leukemia cell lines) |
|
EPB41L3 binds to CADM1 through conserved residues in a well defined hydrophobic pocket in the structural C-lobe of the EPB41L3 FERM domain |
|
ADAM10 mediates endogenous CADM1 shedding |
|
triggers a retrograde signal regulating active zone composition via CADM1 |
|
interacts with ERBB4 and regulates the development of excitatory synapses via the regulation of ERBB4 activity in GABAergic neurons |
|
interaction of CADM1 with ERBB3 inhibits the NRG1-induced ERBB3/ERBB2 signaling in epithelial cells |
| Other morbid association(s)
|
| Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
|
|---|
| tumoral
|
| LOH
|
|
| |
in breast cancer, neuroblastoma, non small cell lung cancer, hepatocellular, nasopharyngeal and pancreatic carcinomas | | tumoral
|
|
|
| loss of function
| |
by promoter hypermethylation in non small cell lung cancer, hepatocellular carcinoma, pancreatic carcinoma, and prostate tumor | | tumoral
|
|
| --low
|
| |
in lung adenocarcinoma associated with lower patient survival, supporting its role as a tumor suppressor and in esophageal squamous cell carcinoma with a poor prognosis | | tumoral
|
|
|
| loss of function
| |
by hypermethylation in premalignant cervical intraepithelial neoplasia by infection with high-risk human papillomavirus (HPV) types, in progression | | tumoral
|
|
| --low
|
| |
in meningioma, associated with decreased survival, and in the atypical meningiomas | | constitutional
|
|
|
| loss of function
| |
causes male infertility | | tumoral
|
|
| --low
|
| |
in metastatic lymph node nasopharyngeal carcinoma | | tumoral
|
|
| --over
|
| |
frequent overexpression in lung adenocarcinoma | | tumoral
|
|
| --over
|
| |
resulted in reduced proliferation and increased levels of CASK and CDH1 at the leading edge of healing wounds | | tumoral
|
|
| --low
|
| |
frequently observed in various cancers, including non-small cell lung cancer (NSCLC) especially in their invasive lesions | | tumoral
|
|
| --low
|
| |
is a critical event in neuroblastoma pathogenesis resulting in tumour progression and unfavourable patient outcome | | tumoral
|
|
| --low
|
| |
by hypermethylation in squamous cell carcinomas (SCCs)of uterine cervix | | tumoral
|
|
| --over
|
| |
in adult T-cell leukemia-lymphoma (ATL) cells | |
| Susceptibility
|
to Autism Spectrum Disorder (ASD) |
| Variant & Polymorphism
other
| mutationslocated in the third immunoglobulin (Ig3) domain essential for homophilic or heterophilic transactive interaction associated to Autism Spectrum Disorder (likely these mutations cause the loss of function, resulting in the impaired synaptogenesis, which is closely associated with the pathogenesis of ASD) |
| 
|
Candidate gene
Marker
Therapy target
|
| | | |
|
| Cadm1-knock out (KO) mice exhibit smaller cerebella with decreased number of synapse of Purkinje cells and some ASD-like symptoms, including impaired ultrasonic vocalization | |
epidermal overexpression of Cadm1 in transgenic mice led to increased autoimmune alopecia susceptibility relative to nontransgenic littermate controls |
