鈣網蛋白是一種多功能蛋白，在內質網管腔內起主要鈣（2+）結合（儲存）蛋白的作用。它也在細胞核中發現，表明它可能在轉錄調節中起作用。鈣網蛋白與合成肽klgfkr結合，后者幾乎與核受體超家族的DNA結合域中的一個氨基酸序列相同。鈣網蛋白與系統性狼瘡和干燥病人的某些血清中的抗體結合，這些血清中含有抗Ro/SSA抗體，在物種間高度保守，位于內質和肌漿網中，可與鈣結合。鈣網蛋白的氨基末端與糖皮質激素受體的DNA結合域相互作用，阻止該受體與其特定的糖皮質激素反應元件結合。鈣網蛋白能抑制雄激素受體與其激素反應性DNA元件的結合，抑制體內雄激素受體和維甲酸受體的轉錄活性，以及維甲酸誘導的神經元分化。因此，鈣網蛋白可以作為調節核激素受體基因轉錄的重要調節劑。系統性紅斑狼瘡與對鈣網蛋白的自身抗體滴度升高有關，但鈣網蛋白不是一種RO/SS-A抗原。早先的論文提到鈣網狀蛋白是一種反滲透/反滲透-A抗原，但這后來被駁倒了。對人鈣網蛋白的自身抗體滴度增加見于患有完全先天性心臟傳導阻滯的嬰兒，包括IgG和IgM兩類。
Calreticulin is a multifunctional protein that acts as a major Ca(2+)-binding (storage) protein in the lumen of the endoplasmic reticulum. It is also found in the nucleus, suggesting that it may have a role in transcription regulation. Calreticulin binds to the synthetic peptide KLGFFKR, which is almost identical to an amino acid sequence in the DNA-binding domain of the superfamily of nuclear receptors. Calreticulin binds to antibodies in certain sera of systemic lupus and Sjogren patients which contain anti-Ro/SSA antibodies, it is highly conserved among species, and it is located in the endoplasmic and sarcoplasmic reticulum where it may bind calcium. The amino terminus of calreticulin interacts with the DNA-binding domain of the glucocorticoid receptor and prevents the receptor from binding to its specific glucocorticoid response element. Calreticulin can inhibit the binding of androgen receptor to its hormone-responsive DNA element and can inhibit androgen receptor and retinoic acid receptor transcriptional activities in vivo, as well as retinoic acid-induced neuronal differentiation. Thus, calreticulin can act as an important modulator of the regulation of gene transcription by nuclear hormone receptors. Systemic lupus erythematosus is associated with increased autoantibody titers against calreticulin but calreticulin is not a Ro/SS-A antigen. Earlier papers referred to calreticulin as an Ro/SS-A antigen but this was later disproven. Increased autoantibody titer against human calreticulin is found in infants with complete congenital heart block of both the IgG and IgM classes.