Antibodies

ABCG1 (ATP-binding cassette sub-family G member 1) is a transporter protein that is primarily involved in macrophage lipid homeostasis. It is a member of the superfamily of ATP-binding cassette (ABC) transporters and localizes to intracellular compartments associated with endoplasmic reticulum and golgi membranes.

p62/SQSTM1 (sequestosome 1) is ubiquitously-expressed cytoplasmic/adaptor protein. SQSTM1 functions as a signaling hub for various signal transduction pathways involved in apoptosis, cell differentiation, apoptosis, immune response, and K+ channel regulation. It is conserved in vertebrates and can be induced by a wide variety of triggers including the proteasomal inhibitor PSI, PGJ2/prostaglandin J2, and the tumor promoting agent phorbol 12-myristate 13-acetate (PMA).

The extracellular matrix (ECM) is a well-structured composite of collagens, proteoglycans, glycoproteins, and growth factors proficient of generating variable measures of tissue tensile potency, from mucosal linings to bones. ECM predominantly comprises the cellular milieu outside the circulation and is established as having a major regulatory effect on cell activity.  There has been a considerable amount of attention towards the disparate conditions in which ECM unambiguously sends or alters signals to the surrounding cells.

Hematopoiesis is a complicated process that is controlled by both intrinsic and extrinsic cellular factors. It is a process of progression by which the diverse cell pedigrees that develop the blood and immune system are spawned from a shared pluripotent hematopoietic stem cell (HSC). Throughout the lifespan of an adult, two distinct hematopoietic systems are present, both resulting through embryonic development but only one of them enduring into adulthood.

The Lin28-Let-7 stem cell differentiation regulatory pathway is responsible for maintaining stem cell pluripotency. Specifically, Lin28 causes uridiylation of the let-7 miRNA precursor, which prevents differentiation processing by Dicer. Instead, the Uridylated let-7 is degraded by a previously unidentified exonuclease protein. In the article “A role for the Perlman syndrome exonuclease Dis3l2 in the Lin28-let-7 pathway” HM Chang, et al.

The biological importance of protein phosphorylation is underlined by the existence of 500 or more protein kinases within the human genome. In most cases, phosphorylation of serine residues creates binding surfaces for a variety of phospho-amino acid binding proteins. Phosphorylation is a key post-translational modification necessary for normal cell signaling and is a key player in cellular function. Phosphorylated proteins mediate cell division, differentiation, signal transduction and other key cell signaling processes.

Synaptonemal Complex Protein 1 (SCP1) is a novel tumor antigen that belongs to the growing family of cancer/testis antigens (CTAs). CTAs are theoretically ideal targets for tumor immunotherapy. Unlike most auto-antigens, CTAs are highly immunogenic, even in the autologous cancer-bearing patients. Furthermore, because of their very restricted normal tissue expression, immunotherapy targeting CTAs is expected to be more specific and less toxic.

Niemann-Pick type C (NPC) disease is a severe cell lipidosis characterized by the accumulation of unesterified cholesterol in the endosomal/lysosomal system. It is a lysosomal storage disorder that affects the viscera and the central nervous system which is caused by the accumulation of cholesterol in lysosomes (1). Niemann-Pick disease type C1 has a highly variable clinical phenotype and clinical features include variable hepatosplenomegaly and severe progressive neurological dysfunction such as ataxia, dystonia and dementia (2).

E-cadherin (also known as Arc-1, uvomorulin, and cell-CAM 120/80) is a calcium-regulated adhesion molecule expressed in most normal epithelial tissues and the loss of E-cadherin can cause dedifferentiation and invasiveness in several cancers (1). Loss of E-Cadherin expression correlated with the invasiveness of carcinoma (2).

FOXP3, a member of forkhead/winged-helix family of transcription factors acts as a "master" regulator for the development and suppressive function of regulatory T cells (Tregs). Its constitutive expression is necessary for the suppressive function of Tregs, and mutation or deficiency of FOXP3 leads to development of autoimmune diseases (1). FOXP3 expression has also been reported in a variety of solid tumors, including melanoma.