SRC
The SRC proto-oncogene, also denoted as c-Src, encodes a cytoplasmic non-receptor tyrosine kinase that serves as the prototype for the Src family of kinases (SFKs), a group of nine related enzymes conserved across vertebrates.[1][2] This 536-amino-acid protein features modular domains including an SH3 domain for protein-protein interactions, an SH2 domain for phosphotyrosine recognition, a kinase domain for catalytic activity, and a regulatory C-terminal tail with a tyrosine residue (Tyr527 in humans) that controls autoinhibition through intramolecular binding.[2][3] Discovered in 1970 as the viral oncogene v-Src from the Rous sarcoma retrovirus, which induces sarcomas in chickens via constitutive kinase activation, the cellular homolog c-Src was identified in 1978 and recognized as the first proto-oncogene, establishing a paradigm for how normal cellular genes can contribute to tumorigenesis when mutated or overexpressed.[1][4] Src integrates signals from diverse receptors, such as integrins, G-protein-coupled receptors, and receptor tyrosine kinases, to orchestrate cytoskeletal dynamics, cell adhesion, migration, proliferation, and survival through phosphorylation of substrates like focal adhesion kinase (FAK) and signal transducer and activator of transcription 3 (STAT3).[5][3] In physiological contexts, Src activity is tightly regulated by C-terminal Src kinase (CSK)-mediated phosphorylation at Tyr527, which maintains an inactive conformation, and dephosphorylation by protein tyrosine phosphatases like PTP1B to enable activation upon stimuli.[2][6] Notable achievements include Src's role in elucidating tyrosine kinase signaling pathways, earning Peyton Rous the 1966 Nobel Prize for discovering tumor-inducing viruses (with implications for Src's viral origins) and advancing targeted therapies, such as the Src/ABL inhibitor dasatinib approved for chronic myelogenous leukemia.[1][7] Controversies surrounding Src center on its therapeutic targeting in solid tumors, where despite correlations with poor prognosis in cancers like colorectal and breast carcinoma due to elevated activity from mutations (e.g., Tyr527Phe) or gene amplification, clinical trials of Src inhibitors like saracatinib have shown limited efficacy as monotherapies, attributed to compensatory pathways and tumor heterogeneity rather than flaws in the underlying biochemical model.[7][8] Academic sources, while empirically grounded in kinase assays and structural biology, occasionally overemphasize Src's universality in oncogenesis amid systemic incentives for grant funding in cancer research, yet first-principles validation via crystallographic studies and knockout models confirms its causal roles in mitogenic signaling independent of such biases.[5][8] Ongoing research explores Src's intersections with metabolism, such as glycolytic flux regulation, positioning it as a potential combinatorial target with immunotherapies.[5]Education
Students' representative council
A students' representative council (SRC) is an elected student body that serves as the primary voice for undergraduates and sometimes postgraduates in university governance, advocating on matters such as academic policies, welfare services, and institutional decision-making.[9] These councils operate independently from university administrations, often with statutory or constitutional recognition to ensure student input into areas like teaching quality, campus facilities, and external relations.[10] Membership typically comprises students elected annually through democratic processes, including representatives from faculties, residences, or affiliated organizations, with leadership roles like president and vice-presidents handling executive functions.[11] The origins of SRCs trace to Scottish universities in the late 19th century, where the first such council formed at the University of Edinburgh in 1884 to coordinate student representation amid growing demands for autonomy in higher education. This model received legal backing via the Universities (Scotland) Act 1889, which formalized SRCs as the recognized representative entities at ancient Scottish institutions like Glasgow and Aberdeen, mandating consultation on student affairs to prevent administrative overreach.[10] By the early 20th century, the structure spread to other Commonwealth countries, adapting to local contexts; for instance, in Australia and New Zealand, similar bodies emerged to address post-World War I expansions in student numbers and calls for democratic input.[12] In functions, SRCs facilitate direct engagement between students and university leadership, often negotiating on fee structures, accommodation standards, and curriculum reforms while organizing events to foster community.[13] In South African universities, SRCs have historically played activist roles, such as mobilizing against apartheid-era exclusions and, more recently, leading campaigns for affordable access, with elections drawing high turnout—e.g., over 20,000 voters at the University of Pretoria in 2024.[14] However, operational challenges persist, including funding dependencies on university grants, which can influence independence, and internal factionalism from political affiliations, as seen in contested elections at institutions like the University of Cape Town.[11] Despite these, SRCs remain central to student agency, with data from Scottish councils showing measurable impacts, such as influencing policy changes in 70% of welfare submissions reviewed annually at Glasgow University.[15] Variations exist regionally: Scottish SRCs emphasize legal parity under ancient acts, limiting their scope to representation without commercial activities, whereas South African counterparts integrate broader social justice mandates, reflecting post-1994 democratic transitions.[16] In both, accountability mechanisms include open meetings and audits, though efficacy depends on turnout; for example, low participation in some elections—under 30% at certain UKZN campuses—highlights engagement gaps.[17] Overall, SRCs embody student self-governance, grounded in empirical needs for collective bargaining rather than administrative deference.Music and entertainment
SRC (band)
SRC was an American psychedelic rock band originating from the Detroit metropolitan area in Michigan, active from 1966 to 1972.[18][19] The group formed as The Fugitives, a Birmingham-based garage band featuring brothers Gary Quackenbush on guitar and Glenn Quackenbush on organ, alongside drummer E.G. Clawson; they recruited vocalist Scott Richardson in 1966, leading to the extended name Scot Richard Case before shortening to SRC in 1968.[19][18] Initially playing local clubs, SRC gained prominence through frequent appearances at Detroit's Grande Ballroom and other venues during the city's vibrant rock scene, sharing bills with acts like The Who, for whom they substituted during a 1967 equipment failure that fostered a lasting friendship.[20][18] The band's core lineup during their Capitol Records era consisted of Scott Richardson (lead vocals), Gary Quackenbush (guitar, backing vocals), Glenn Quackenbush (keyboards, backing vocals), E.G. Clawson (drums), and Max Ross (bass, replacing early member Robin Dale after the debut album).[19][21] Their sound blended psychedelic rock with progressive elements, characterized by intricate arrangements, organ-driven textures, and Richardson's dynamic vocals; early singles like "Stop" (1966, as The Fugitives) and "Black Sheep" reflected garage rock roots, evolving into heavier, more experimental tracks on later releases.[18][21] SRC signed with Capitol in 1968 after label interest sparked by their regional popularity and a connection to producer John Rhys Eddins, who helmed their sophomore effort.[18] SRC released three studio albums on Capitol: the self-titled SRC in November 1968, featuring tracks like "Black Sheep" and "Reflections"; Milestones in spring 1969, produced by Eddins and the band, showcasing progressive shifts with songs such as "Marionette"; and Traveler's Tale in 1970, their most ambitious work incorporating orchestral elements on cuts like "Everytime" and "Stay with Me Tonight."[18][22] Despite critical praise for their musicianship—often compared to contemporaries like Cream or early prog acts—the albums achieved limited commercial success, with none charting nationally.[21] The band toured extensively, including Midwest circuits and East Coast dates, but internal tensions and label disinterest led to their 1971 dropout from Capitol and dissolution by 1972.[19] Post-breakup, members pursued varied paths: Richardson fronted other projects, while the Quackenbush brothers contributed to session work. A posthumous compilation, Lost Masters, surfaced in 2000, compiling unreleased 1970-1971 recordings intended for a fourth album, highlighting unfinished material with psychedelic and hard rock influences.[22] SRC's legacy endures in Michigan rock history, recognized for pioneering the region's fusion of raw energy and sophistication; they were inducted into the Michigan Rock and Roll Legends Hall of Fame in 2008.[18] Their influence persists among collectors and enthusiasts of late-1960s American psychedelia, with reissues maintaining availability of their catalog.[21]SRC (album)
SRC is the eponymous debut studio album by the American rock band SRC, released in 1968 by Capitol Records.[23] Recorded at Tera Shirma Studios, the album showcases the band's origins in the Detroit rock scene, blending heavy psychedelic rock with progressive elements through complex compositions and fuzz guitar work.[24] The lineup featured vocalist Scott Richardson, guitarist Gary Quackenbush, keyboardist Glenn Quackenbush, drummer E.G. Clawson, and bassist Robin Dale, marking the only SRC release with Dale before his departure.[25] All tracks were written by the band members collectively.[23] The album's sound draws from the late-1960s psychedelic and proto-progressive styles prevalent in the Midwest underground scene, characterized by extended instrumental passages, harmonies, and tracks like "Black Sheep" that highlight shiver-inducing backing vocals and heavy riffing.[26] Clocking in at approximately 35 minutes, it includes eight original songs divided across two sides, with no singles initially charted from the release.[27] Upon its U.S. issuance, SRC generated excitement among fans and critics for its ambitious arrangements, though commercial success was limited amid the competitive rock market.[28]Track listing
All songs written by SRC.| No. | Title | Length |
|---|---|---|
| 1. | "Black Sheep" | 4:46 |
| 2. | "Daystar" | 4:24 |
| 3. | "Exile" | 4:20 |
| 4. | "Marionette" | 3:58 |
| 5. | "Onesimpletask" | 5:32 |
| 6. | "Paragon Council" | 4:00 |
| 7. | "Refugeve" | 3:38 |
| 8. | "Interval" | 5:13 |
SRC Records
SRC Records, operating as Street Records Corporation, was an American hip-hop record label established in 2002 by music executive Steve Rifkind following the closure of his prior venture, Loud Records, by Sony.[29] Distributed through Universal Motown as part of Universal Music Group, the label focused on urban and hip-hop acts, building on Rifkind's experience in signing influential artists from the genre's street-oriented scene.[29][30] The imprint achieved notable success with signings including Akon, whose 2004 debut album Trouble—featuring hits like "Locked Up" and "Lonely"—sold over 900,000 copies in the U.S. and earned platinum certification from the RIAA.[29] Other roster highlights encompassed Asher Roth, whose 2009 release Asleep in the Bread Aisle debuted at number five on the Billboard 200 with over 165,000 first-week sales; Ray J; and Melanie Fiona.[29] SRC also housed imprints and collaborated on projects amplifying emerging talent in hip-hop production and artist development.[30] Operations ceased effectively in 2012 when Rifkind exited his Universal deal more than a year early, driven by disputes over business strategy and creative autonomy amid shifting industry priorities toward digital distribution and major-label consolidations.[29] The label's catalog remains under Universal's management, contributing to Rifkind's legacy in hip-hop entrepreneurship, though it did not sustain independent activity post-departure.[31]Biology and medicine
Proto-oncogene tyrosine-protein kinase Src
Proto-oncogene tyrosine-protein kinase Src, also known as c-Src, is a non-receptor tyrosine kinase encoded by the SRC gene on human chromosome 20q12-q13.[1] This 536-amino-acid protein belongs to the Src family kinases (SFKs), characterized by modular domains including an N-terminal myristoylation site for membrane association, Src homology 3 (SH3) and Src homology 2 (SH2) domains for protein-protein interactions, a linker region, a bilobal kinase domain, and a C-terminal regulatory tail.[32] The kinase domain catalyzes phosphorylation of tyrosine residues on substrate proteins, facilitating downstream signaling in pathways involved in cytoskeletal organization and cell motility.[33] The identification of Src originated from studies of Rous sarcoma virus (RSV), isolated by Peyton Rous in 1911 as a filterable agent causing sarcomas in chickens, marking the first demonstration of a viral oncogene.[34] In 1977, Joan Brugge and Raymond Erikson identified the RSV transforming protein v-Src and associated it with protein kinase activity; subsequent work in 1979-1980 by Tony Hunter's group revealed that v-Src specifically phosphorylates tyrosine residues, establishing tyrosine phosphorylation as a key regulatory mechanism and Src as the first known tyrosine kinase.[35] [36] The cellular counterpart, c-Src, was cloned in 1981 as the proto-oncogene homolog of v-Src, differing primarily in the C-terminal regulatory sequence that renders c-Src subject to autoinhibition, preventing constitutive activity observed in the viral form.[37] c-Src function centers on transducing signals from cell surface receptors, such as integrins and growth factor receptors, to intracellular effectors, thereby regulating processes including cell adhesion, migration, proliferation, differentiation, and survival.[33] In non-transformed cells, c-Src activity is tightly controlled through intramolecular interactions and phosphorylation: C-terminal Src kinase (Csk) phosphorylates Tyr527 in the regulatory tail, promoting SH2 domain binding to this site and kinase domain occlusion by the SH3 domain, maintaining an inactive conformation.[32] Activation occurs via dephosphorylation of Tyr527 or autophosphorylation at Tyr416 in the kinase domain activation loop, often triggered by upstream signals like integrin engagement.[38] Dysregulated c-Src contributes to pathologies beyond cancer, including enhanced osteoclast activity in bone resorption and microglial activation in neuroinflammation.[39] In oncogenesis, c-Src transforms from proto-oncogene to oncogene through mutations, overexpression, or loss of regulatory phosphorylation, as seen in up to 80% of colon cancers where SRC mRNA levels correlate with disease progression.[5] Hyperactive c-Src drives tumor invasion, angiogenesis, and metastasis by phosphorylating targets like focal adhesion kinase (FAK) and paxillin, disrupting adherens junctions, and promoting epithelial-mesenchymal transition.[40] Therapeutic targeting exploits this: dasatinib, a small-molecule inhibitor binding the ATP site of Src and Abl kinases with IC50 values of 0.5 nM and 0.6 nM respectively, was approved by the FDA in 2006 for chronic myeloid leukemia and shows preclinical efficacy in Src-dependent solid tumors by reducing proliferation and inducing apoptosis.[41] [42] Clinical trials, such as phase II studies in prostate and breast cancers, demonstrate partial responses in Src-overexpressing subsets, though resistance via compensatory pathways like MAPK activation limits broad utility.[43]Src family kinase
The Src family kinases (SFKs) are a group of nine non-receptor tyrosine protein kinases in mammals, including Src, Fyn, Yes, Lck, Hck, Fgr, Blk, Lyn, and Frk, which play critical roles in signal transduction pathways regulating cellular processes such as proliferation, differentiation, migration, adhesion, and survival.[44] These kinases were first identified through the v-Src oncoprotein from Rous sarcoma virus, with the cellular homolog c-Src discovered in 1978 as the first proto-oncogene.[45] SFKs transduce signals from cell surface receptors, including growth factor receptors, integrins, and G-protein-coupled receptors, by phosphorylating tyrosine residues on substrate proteins.[46] Structurally, SFKs share a conserved modular architecture consisting of an N-terminal myristoylation site for membrane anchoring, a unique domain varying among members, Src homology 3 (SH3) and Src homology 2 (SH2) domains for protein-protein interactions, a linker region, a bilobal kinase domain, and a C-terminal regulatory tyrosine residue.[47] The SH3 domain binds proline-rich sequences, while the SH2 domain recognizes phosphotyrosine motifs, enabling recruitment to activated receptors and downstream effectors.[48] Kinase activity is tightly regulated: inhibitory phosphorylation at the C-terminal tyrosine (e.g., Tyr527 in Src) by kinases like Csk or Chk promotes an intramolecular clamp with the SH2 domain, maintaining an inactive conformation; dephosphorylation or activating phosphorylation at the kinase domain's activation loop tyrosine (e.g., Tyr416 in Src) shifts to an open, active state.[49] This dynamic regulation allows rapid responses to extracellular cues, with SFKs often associating with lipid rafts for localized signaling.[50] In physiological contexts, SFKs mediate diverse functions across cell types: Lck and Fyn drive T-cell receptor signaling for immune activation; Lyn and Hck regulate B-cell and myeloid cell responses; Src, Fyn, and Yes influence neuronal synaptic plasticity and cytoskeletal dynamics via focal adhesion kinase interactions.[44] Dysregulation, such as overexpression or activating mutations, contributes to pathologies including solid tumors, where SFKs promote epithelial-mesenchymal transition, invasion, and metastasis through pathways like FAK/PI3K/Akt and STAT3.[51] For instance, elevated Src activity correlates with poor prognosis in colorectal and breast cancers, prompting development of inhibitors like dasatinib, approved in 2006 for chronic myelogenous leukemia but explored in solid tumor trials.[52] Cardiovascular roles include SFK involvement in platelet aggregation and vascular smooth muscle contraction, with inhibition reducing thrombosis risk.[53]Computing and technology
Source code (src)
In software development, "src" is a standard abbreviation for "source," commonly used to denote directories containing human-readable source code files that define program logic and are processed by compilers, interpreters, or build tools to produce executable binaries or runtime artifacts.[54][55] This convention organizes project structures by isolating editable code from derived outputs, such as compiled binaries in a "bin" or "dist" folder, facilitating version control, collaboration, and automated builds.[56][57] The "src" directory emerged as a best practice in the 1990s alongside structured project layouts in languages like C and Java, where source files (e.g., .java, .c) reside under src/ to mirror package hierarchies and avoid cluttering the project root.[55] In Java, for instance, the Maven build tool enforces src/main/java for application code and src/test/java for tests, ensuring reproducible builds independent of IDE-specific paths.[55] Similarly, in JavaScript and Node.js projects, src/ holds unminified scripts before bundling into distribution folders, as seen in tools like Webpack or npm workflows.[54] In Python packaging, the "src" layout—placing modules under src/package_name/—gained prominence in the 2010s to prevent accidental imports of development scripts or tests during editable installs via pip, contrasting with "flat" layouts where code sits directly in the project root.[58][59] Frameworks like Next.js and Plasmo explicitly support optional src/ relocation of app or page routers for cleaner root directories, maintaining compatibility with tools like TypeScript.[60][61] This approach enhances modularity, especially in monorepos or libraries, by enforcing that only explicitly declared packages are importable.[58] The ".src" file extension, less standardized than the directory convention, denotes source code in niche contexts, such as DataFlex applications or legacy Forth compilers, where files store uncompiled program text for processing into executables.[62][63] However, it is not a universal standard like .c or .py, often varying by tool or language (e.g., KUKA robot SRC files for executable code).[64] Adoption of "src" universally promotes portability across ecosystems, reducing errors in builds and deployments, though some minimal projects omit it for simplicity in single-file setups.[58][55]SRC command
The System Resource Controller (SRC) in IBM AIX is a facility for managing subsystems, which are daemon processes or groups of related processes that perform system services.[65] It provides a unified interface for administrators to start, stop, refresh, trace, and query the status of these subsystems, along with error notification and recovery mechanisms.[65] The SRC operates through thesrcmstr daemon, which is automatically initiated by the init process during system boot as defined in /etc/inittab, and requires root privileges for most operations.[65] Subsystems are defined using structures from /usr/include/sys/srcobj.h and can include subservers—child processes controlled by a parent subsystem—or groups for collective management, such as the tcpip group encompassing networking daemons.[65][66]
SRC commands facilitate inter-process communication via signals for basic control (e.g., stop requests), or advanced methods like sockets or IPC message queues for bidirectional interaction, requiring linkage to libsrc.a and headers like /usr/include/spc.h.[65] Optional features include status reporting, tracing for debugging, and refresh operations to reload configuration without restarting.[65] For instance, signals use one-way schemes where subsystems respond only to termination requests, while socket-based communication enables full request-response cycles.[67]
Key SRC commands include:
startsrc: Initiates a subsystem, subserver, or group, passing arguments if specified; example:startsrc -s nfsdto launch NFS daemons as configured in scripts.[68][65]stopsrc: Halts resources using signals like SIGTERM (SIGNORM for graceful shutdown), SIGKILL (SIGFORCE for immediate termination), or SIGCANCEL; example:stopsrc -s [inetd](/page/Inetd)to stop the inetd superdaemon.[68][65]lssrc: Queries status, with options like-sfor a single subsystem (e.g.,lssrc -s [sendmail](/page/Sendmail)),-gfor groups (e.g.,lssrc -g tcpip), or-lfor detailed output including process IDs and arguments.[65][69]refresh: Reloads subsystem configuration without downtime, if supported; example:refresh -s [named](/page/BIND)for the BIND name server.[65]tracesonandtracesoff: Enable or disable kernel tracing for a subsystem, aiding diagnostics.[65]
srcmstr is invoked with the -r flag, though local operations predominate for security.[65] Developers integrate SRC via APIs for custom subsystems, enhancing reliability in enterprise Unix deployments.[65]