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FLASH GENE

Symbol

IL1B

contributors: mct - updated : 02-06-2019

HGNC name	interleukin 1, beta
HGNC id	5992

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_000576 7 - 1498 NP_000567 - 269 - 1997 9169134

EXPRESSION

Type	restricted

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Cardiovascular vessel       predominantly Digestive esophagus       highly   liver       highly   pharynx       lowly Lymphoid/Immune spleen       lowly Nervous brain       lowly Respiratory lung       highly

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Blood / hematopoietic bone marrow     lowly Connective bone     lowly

cells

System Cell Pubmed Species Stage Rna symbol Lymphoid/Immune macrophage

cell lineage
cell lines	osteoblastic, gastric carcinoma predominantly
fluid/secretion	blood

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	a 92 amino acids interleukin-1 propeptide domain
	an interleukin-1 homologes domain

mono polymer

monomer

isoforms

Precursor

an 153 amino acids mature peptide (17.4 kDa)

HOMOLOGY

interspecies	homolog to rattus Il1b (68.05 pc)
	homolog to murine Il1b (69.55 pc)

intraspecies

paralog to IL1A

Homologene

FAMILY	interleukin 1 family
	IL-1 family

CATEGORY

immunity/defense , signaling cytokine

SUBCELLULAR LOCALIZATION	extracellular
	intracellular
	intracellular,cytoplasm,cytosolic,granule

basic FUNCTION	potential initiator and amplificator of the immune and inflammatory response
	putatively stimulating osteoclastogenesis
	inducing the association of TRAF6 with IRAK1, involved in the inflammatory response
	is capable of decreasing insulin-induced glucose transport
	involved in the negative regulation of cell proliferation
	IL1B, released from dying cells, promotes the recruitment and retention of macrophages
	autophagy has a potentially pivotal role to play in the induction and regulation of inflammatory responses by innate immune cells, largely driven by IL1A, IL1B and its consequential effects on IL23A secretion
	the effects of IL1B and insulin on FOXO1 are additive, albeit independent, with respect to the distribution of FOXO1 between the nucleus and cytosol
	MYLK is a key regulator involved in endothelial hyperpermeability, and IL1B has been shown to mediate MYLK-dependent barrier dysfunction in epithelia
	IL1A, IL1B are important participants in the age-related exhaustion of ovarian reserve in mammalian, possibly by enhancing the expression of inflammatory genes and promoting apoptotic pathways
	IL1A, IL1B are potent regulators of the innate immune system important for host defense but are also associated with injury and disease in the brain
	IL1A and IL1B are key players in the innate immune system
	IL1B promotes nuclear DNASE1 translocation in an endonuclease-inactive form
	matricellular protein RSPO3 is a mediator of endothelial hyperpermeability that can act in synergy with the inflammatory mediator IL1B

CELLULAR PROCESS	cell life, differentiation
	cell life, proliferation/growth
	cell life, cell death/apoptosis

PHYSIOLOGICAL PROCESS

immunity/defense , inflammation

text	host response to pathogens in the NF-kappa B signaling pathway

PATHWAY

metabolism

signaling

signal transduction

NF-kappa B signaling pathway

a component

INTERACTION

DNA

RNA

small molecule

protein	upregulating SLAM (signaling lymphocyte activation molecule) on mature dendritic cells
	upregulating ADAMTS1 in stromal cells
	IL1A stimulates cardiac myofibroblasts (CMF) to express IL1B, TNF, and IL6 via specific signaling pathways
	IL1B induced SMAD7 negatively regulates gastrin expression
	IL1B, IL1A both bind to the same IL1 receptor (IL1R1) and are potent proinflammatory cytokines
	IL1B directly binds IL1A, thus identifying IL1B as a shuttle for another proinflammatory cytokine
	a major proinflammatory cytokine, IL1B, can facilitate local progesterone metabolism in a cell type critical for maintaining uterine cervical structure via regulating expression of AKR1C1 and AKR1C2
	IL1B regulates FOXO1 activity through a novel SMPD3-dependent pathway
	IL1B counteracts the AKT1-mediated insulin signals by increasing the overall cellular FOXO1 content and augmenting its nuclear localization
	NLRP3 is a key component of one of several distinct cytoplasmic multiprotein complexes (inflammasomes) that mediate the maturation of the proinflammatory cytokine IL1B by activating CASP1
	TLR3 stimulation in keratinocytes induces a CASP4 dependent release of pro-IL1B, but further processing to active IL1B is limited
	secretion of IL1A, IL1B, IL12B, and CCL4 occurs during gelatinase degranulation, a process controlled by STX3
	NFKB1 may be involved in IL1B-induced activation of ADAMTS9 in human chondrocytes
	in the presence of CASP1, CASP8 acts as a positive modulator of the NLRP3-dependent CASP1 signaling cascades that drive both IL1B production and pyroptotic death
	PLIN2 inhibits insulin&
	8209;induced glucose uptake by activating NLRP3, CASP1 and IL1B, leading to a decreased IRS1 expression
	CASP4 and caspase-5 mediate IL1A and IL1B release from human monocytes after lipopolysaccharide (LPS) stimulation
	IL36G expression was induced by the combination of IL1B and TNF via activation of MAPKs and transcription factors, NFKB1 and JUN in colonic myofibroblasts
	PGAM5 is a mitochondrial phosphatase that has been reported to function downstream of RIPK3 to promote necroptosis and IL1B secretion
	IL1B regulates NOTCH1 and NOTCH4 activity in opposite directions, consistent with a selective targeting of NOTCH1 in inflamed endothelium
	NLRC4-driven IL1B production is critical for the progression of Diabetic Nephropathy
	new roles for CD14 and IL1B linking inflammatory dendritic cells to IL17A production in memory CD4+ T cells
	CASP4 physically interacts with CASP1 and is believed to be a proinflammatory caspase that can induce the inflammatory form of programmed cell death (pyroptosis) and the release of mature interleukin IL1B
	IL1B increases AMTN gene transcription in gingival epithelial cells mediated through CEBP1, CEBP2, and YY1 elements in the human AMTN gene promoter

cell & other

REGULATION

activated by

after cleavage by caspase 1

repressed by

heat shock factor 1 through physical interaction with CEBPB

Other

IL1A and IL1B polyubiquitination and proteasomal degradation are central mechanisms in the regulation of intracellular IL1 levels in dendritic cells

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral     --over   in multiple myeloma constitutional     --over   mRNA levels of NLRC4, NLRP12, and IL1B were significantly upregulated in Kawasaki disease (KD) patients compared to the controls

Susceptibility

susceptibility factor to inflammatory bowel diseases and temporal lobe epilepsy susceptibility to schizophrenia and bipolar disorder to bone involvement in celiac disease to Chronic kidney disease (CKD) and periodontitis (PD) to diabetes

Variant & Polymorphism SNP , other	SNP 511 susceptibility to asthma exclusively in males and to schizophrenia and bipolar disorder
	increased in febrile seizures
	gene cluster polymorphisms are related to velocity of tooth translation
	IL1B rs1143634(G-->A) was associated with higher blood glucose than the major allele: 5.37, 5.41, and 5.48 mmol/liter for the GG, AG, and AA genotypes, respectively
	carriers of allele T of the interleukin-1beta gene (IL1B-511T) had a significantly lower bone mass at the total skeleton level in celiac disease
	association of IL1B alleles with susceptibility to CKD and PD

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS