Acts as an adapter protein that mediates cell signaling pathways involved in cellular functions such as cell adhesion and migration, tissue organization, and the regulation of the immune response (PubMed:20505138, PubMed:20881139, PubMed:20956287). Plays a role in integrin-mediated cell adhesion through BCAR1-CRK-RAPGEF1 signaling and activation of the small GTPase RAP1 (By similarity). Promotes cell migration and invasion through the extracellular matrix (PubMed:20881139). Required for marginal zone B-cell development and thymus-independent type 2 immune responses (PubMed:20505138, PubMed:20956287). Mediates migration and adhesion of B cells in the splenic marginal zone via promoting hyperphosphorylation of NEDD9/CASL (PubMed:20505138). Plays a role in CXCL13-induced chemotaxis of B-cells (PubMed:20505138, PubMed:20956287). Plays a role in the migration of olfactory sensory neurons (OSNs) into the forebrain and the innervation of the olfactory bulb by the OSN axons during development (PubMed:20881139). Required for the efficient tyrosine phosphorylation of BCAR1 in OSN axons (PubMed:20881139). Important regulator of chemokine-induced, integrin-mediated T lymphocyte adhesion and migration, acting upstream of RAP1 (PubMed:17174122). Required for tissue-specific adhesion of T lymphocytes to peripheral tissues (PubMed:17174122). Required for basal and CXCL2 stimulated serine-threonine phosphorylation of NEDD9 (PubMed:17174122). May be involved in the regulation of T-cell receptor-mediated IL2 production through the activation of the JNK pathway in T-cells (PubMed:12486027). May be involved in the BCAR1/CAS-mediated JNK activation pathway. Component of a complex comprised of SH2D3C, BCAR1/CAS, and CRK (By similarity). Within the complex, interacts with CRK and (via C-terminus) with BCAR1/CAS (via C-terminus) (PubMed:10692442, PubMed:17174122). Interacts with NEDD9/HEF1 (PubMed:20956287). Interacts with EPHB2 (PubMed:10542222). Interacts with NEDD9/HEF1 (PubMed:10692442, PubMed:17174122). Interacts with BCAR1/CAS (PubMed:10692442). Interacts with PTK2B (PubMed:12486027). Interacts (via C-terminus) with BCAR1/CAS (via C-terminus) (PubMed:10692442). Interacts with IGF1 (PubMed:20881139). Associated with the membrane when EGF-stimulated (PubMed:10692442). Expressed at the cortical actin ring in B cells (PubMed:20956287). Expressed in the olfactory bulb and olfactory sensory neurons (at protein level) (PubMed:20881139). Expressed in B cells (at protein level) (PubMed:20505138, PubMed:20956287). Expressed in T lymphocytes (PubMed:17174122). Expressed in hematopoietic cells from spleen, lymph node and thymus (at protein level) (PubMed:10542222, PubMed:10692442, PubMed:12486027). Expressed weakly in the lung (at protein level) (PubMed:10692442). Expressed in the brain, lung, kidney, and weakly expressed in the liver and lung (at protein level). Expressed in the developing OSNs at dpc 13.5 and 14.5 with reduced expression at dpc 16.5. The C-terminal Cdc25-homology/Ras-GEF domain adopts a closed conformation rendering it incapable of carrying out canonical exchange factor function, this closed conformation is required for interaction with BCAR1. Phosphorylated by MAPK/ERK upon T-cell receptor stimulation in T-cells. In one study knockout mice are viable and born at the expected Mendelian rate (PubMed:20505138). In another study the majority of knockout mice die after birth, those that survive show severe lamination defects and loss of cellular organization in their olfactory bulb, with a reduction in gonadotropin-releasing hormone in the preoptic region of the hypothalamus (PubMed:20881139). Mice that die at birth are morphologically normal apart from a marked reduction in the size of the olfactory bulb, which exhibits abnormal cellular organization in the outer layers and a lack of innervation of OSNs (PubMed:20881139). At dpc 16.5 OSNs fail to extend into the marginal zone of the forming olfactory bulb from the basement membrane, and show a reduction in tyrosine phosphorylated BCAR1 (PubMed:20881139). Decrease in B cells in the splenic marginal zone (PubMed:20505138, PubMed:20956287). It is unclear if the knockout of Sh2d3c causes lethality (PubMed:20505138, PubMed:20881139). One report in genetic knockout mice suggests it is viable (PubMed:20505138). Another report in the same strain but a different genetic knockout model suggests lethality (PubMed:20881139).