Plays an important role in the loading of the cohesin complex on to DNA (PubMed:29094699). Forms a heterodimeric complex (also known as cohesin loading complex) with MAU2/SCC4 which mediates the loading of the cohesin complex onto chromatin. Plays a role in cohesin loading at sites of DNA damage. Its recruitment to double-strand breaks (DSBs) sites occurs in a CBX3-, RNF8- and RNF168-dependent manner whereas its recruitment to UV irradiation-induced DNA damage sites occurs in a ATM-, ATR-, RNF8- and RNF168-dependent manner (By similarity). Along with ZNF609, promotes cortical neuron migration during brain development by regulating the transcription of crucial genes in this process. Preferentially binds promoters containing paused RNA polymerase II. Up-regulates the expression of SEMA3A, NRP1, PLXND1 and GABBR2 genes, among others (PubMed:28041881). Heterodimerizes with MAU2/SCC4 to form the cohesin loading complex (By similarity). The NIPBL-MAU2 heterodimer interacts with the SMC1A-SMC3 heterodimer and with the cohesin complex composed of SMC1A, SMC3, RAD21 and STAG1. Interacts directly (via PxVxL motif) with CBX3 and CBX5 (By similarity). Interacts with ZNF609 (via N-terminus) (PubMed:28041881). Interacts with the multiprotein complex Integrator (PubMed:28041881). Spermatocytes and oocytes (at protein level). Widely expressed at 9.5 and 10.5 dpc, with notable accumulations in limb bud, branchial arch and craniofacial mesenchyme. These regions are involved in patterning of the skeleton and soft tissues of the limbs, jaw and face. Expressed in the developing brain, with enrichment in the ventricular zone at 14.5 dpc (PubMed:28041881). Contains one Pro-Xaa-Val-Xaa-Leu (PxVxL) motif, which is required for interaction with chromoshadow domains. This motif requires additional residues -7, -6, +4 and +5 of the central Val which contact the chromoshadow domain. The C-terminal region containing HEAT repeats and Pro-Xaa-Val-Xaa-Leu (PxVxL) motif are involved in the recruitment of NIPBL to sites of DNA damage. Deletion of NIPBL in mouse liver leads to strong depletion of chromatin-bound cohesin and marked reorganization of chromosomal folding. Cells retain transcriptionally active (type A) and transcriptionally inactive (type B) compartments, but lose topologically associating domains (TADs) patterns and TAD-associated peaks of contact enrichment across the whole genome. The compartmentalization of chromatin in cells lacking NIPBL is enhanced around 1.8-fold compared with controls. Belongs to the SCC2/Nipped-B family.