Pathway candidateNCBI-verifiedprotein-coding

BCL2L1

BCL2 like 1

NCBI Gene: 598 Ensembl GeneCards UniProt: Q07817

Pathway candidate — not linked to PFS or PSSD by any record here

BCL2L1 is in the library because it belongs to the general physiology family. No study, report or commentary in the corpus names it, so a variant in BCL2L1 is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome 20 (general physiology). The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities.

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: Bcl-2-like protein 1
Function: Potent inhibitor of cell death. Inhibits activation of caspases. Appears to regulate cell death by blocking the voltage-dependent anion channel (VDAC) by binding to it and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. Also acts as a regulator of G2 checkpoint and progression to cytokinesis during mitosis. Isoform Bcl-X(L) also regulates presynaptic plasticity, including neurotransmitter release and recovery, number of axonal mitochondria as well as size and number of synaptic vesicle clusters. During synaptic stimulation, increases ATP availability from mitochondria through regulation of mitochondrial membrane ATP synthase F(1)F(0) activity and regulates endocytic vesicle retrieval in hippocampal neurons through association with DMN1L and stimulation of its GTPase activity in synaptic vesicles. May attenuate inflammation impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release. Isoform Bcl-X(S) promotes apoptosis.
Subcellular location: Mitochondrion inner membrane; Mitochondrion outer membrane; Mitochondrion matrix; Cytoplasmic vesicle, secretory vesicle, synaptic vesicle membrane; Cytoplasm, cytosol; Cytoplasm, cytoskeleton, microtubule organizing center, centrosome; Nucleus membrane.
Tissue specificity: Bcl-X(S) is expressed at high levels in cells that undergo a high rate of turnover, such as developing lymphocytes. In contrast, Bcl-X(L) is found in tissues containing long-lived postmitotic cells, such as adult brain.

Source: UniProtKB/Swiss-Prot Q07817, release 2026_03, licensed CC BY 4.0. This is the protein’s normal biology, not evidence about post-drug syndromes; associated conditions are inherited disorders of the gene, not PFS, PSSD or PRSD.

Why its pathway is in the library

Established roles outside the core post-drug-syndrome pathways; no direct PFS/PSSD link established — included for completeness.

Written for the whole general physiology family, not for BCL2L1 specifically.

Mentioned in 0 corpus records

No corpus record names BCL2L1 directly yet. It is in the library because it sits in a pathway the corpus tracks (General physiology).

Also in general physiology

All 3 genes

Browse by family on the gene families page.

Gene summary

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: Bcl-2-like protein 1
Function: Potent inhibitor of cell death. Inhibits activation of caspases. Appears to regulate cell death by blocking the voltage-dependent anion channel (VDAC) by binding to it and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. Also acts as a regulator of G2 checkpoint and progression to cytokinesis during mitosis. Isoform Bcl-X(L) also regulates presynaptic plasticity, including neurotransmitter release and recovery, number of axonal mitochondria as well as size and number of synaptic vesicle clusters. During synaptic stimulation, increases ATP availability from mitochondria through regulation of mitochondrial membrane ATP synthase F(1)F(0) activity and regulates endocytic vesicle retrieval in hippocampal neurons through association with DMN1L and stimulation of its GTPase activity in synaptic vesicles. May attenuate inflammation impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release. Isoform Bcl-X(S) promotes apoptosis.
Subcellular location: Mitochondrion inner membrane; Mitochondrion outer membrane; Mitochondrion matrix; Cytoplasmic vesicle, secretory vesicle, synaptic vesicle membrane; Cytoplasm, cytosol; Cytoplasm, cytoskeleton, microtubule organizing center, centrosome; Nucleus membrane.
Tissue specificity: Bcl-X(S) is expressed at high levels in cells that undergo a high rate of turnover, such as developing lymphocytes. In contrast, Bcl-X(L) is found in tissues containing long-lived postmitotic cells, such as adult brain.