A cell wall protein involved with PadA in host cell interactions required for colonization and pathogensis (Probable) (PubMed:19884334, PubMed:27616700). Mediates hemagglutination and adherence to ghst glycoproteins (PubMed:11854202). Recognizes fetuin-A (AHSG), a highly glycosylated human plasma protein, also involved in recognition of human platelets, probably via platelet glycoprotein Ib alpha (GP1BA) (PubMed:19884334). Acts in concert with PadA to promote binding to glycosylated human fibronectin (FN1) and vitronectin (VTN), and biofilm formation. Plays a major role in fibronectin and vitronectin binding; binding is mediated by glycosylated regions. Probably mediates interaction of PadA with resting platelets (PubMed:27616700). Has a short (SR1) and long (SR22) Ser-rich region separated by 2 non-repeats regions (NR1 and NR2). SR2 is comprised of 113 inexact repeats of SASTSASVSASE (PubMed:11854202). SR2 is thought to extend about 0.2 um away from the cell surface (Probable). SR1, NR2 and SR2 are essential for Hsa-mediated hemagglutination and for binding to sialoglycoconjugates (fetuin and NeuAc-alpha-2-3Gal-beta-1-4(Glc)-HSA); removal of the N- or C-terminus of SR2 (residues 448-1459 or 1092-2143 respectively) still allows binding and hemagglutination (PubMed:15213130). The protein is glycosylated in vivo; constructs without SR1 and SR2 are not glycosylated. Loss of bacterial-mediated red blood cell hemagglutination, no bacterial adhesion to glycoconjugates with alpha-2-3 sialic acid termini (PubMed:11854202). No longer aggregates human platelets (PubMed:15213130). Bacteria no longer bind human fetuin. Bacteria bind less well to human platelets. Triple sspA-sspB-hsa deletion no longer causes human platelet aggregation; a single hsa deletion aggregates platelets normally. Significantly reduced binding to human glycocalicin (GP1BA, the shed form of platelet glycoprotein Ib alpha) (PubMed:19884334). No change in platelet spreading on S.gordonii (PubMed:21071690). Single mutant no longer binds to vitronectin (VTN) and fibronectin (FN1), slightly less well to salivary pellicle and makes less biofilm on salivary pellicle. Double hsa-padA deletions bind less well to human platelets than does the single padA deletion and make no biofilm on salivary pellicle (PubMed:27616700). S.gordonii, a commensal oral cavity bacteria, is among the bacteria most frequently identified as being the primary etiological agents of subacute infective endocarditis (found in 13% of cases). Belongs to the serine-rich repeat protein (SRRP) family.